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THE 


Circulatory Disturbances 

OF THE 

Extremities 

INCLUDING GANGRENE , VASOMOTOR AND 
TROPHIC DISORDERS 


BY 

LEO BUERGER, M.A., M.D. 

NEW YORK CITY 


WITH 192 ILLUSTRATIONS 
FIVE IN COLORS 


PHILADELPHIA AND LONDON' 

W. B. SAUNDERS COMPANY 


1924 





Copyright, 1924, by W. B. Saunders Company 


* 


MADE IN TJ. S. A. 





TO 


DR. WILLIAM J. MAYO 
whose masterly surgery has stimulated 

and to 

DR. EMANUEL LIBMAN 
whose unusual medical insight has inculcated 


a spirit of research 


THIS OLUME IS RESPECTFULLY INSCRIBED 



•S* » i 







PREFACE 


Perhaps in no other department of medicine has clinical diagnosis offered 
greater difficulties to the practitioner than in the domain of circulatory, vaso¬ 
motor, and trophic disturbances of the extremities. When the author began 
his pathological studies of the vessels of the extremities in gangrene from 
whatever cause some eighteen years ago, he was not a little surprised to note 
what confused notions regarding clinical classification existed in the minds of 
some of the best internists, neurologists, and surgeons. Chronic rubor 
associated with obstructive arterial disease was reported as evidencing an 
identity of pathogenesis in such diverse clinical entities as erythromelalgia, 
Raynaud’s disease, and thrombo-angiitis obliterans; and these three essenti¬ 
ally different maladies were even described as of similar origin. 

Whilst the recognition of thrombo-angiitis obliterans with its kaleido¬ 
scopic manifestations has had a clarifying influence, and whilst descriptions 
of its varied symptomatology may have contributed to a better insight into 
what phenomena are of neurogenic and what are of purely mechanical and 
hydrostatic motivation, the subject seems for many to be still enshrouded 
in much mystery. For, it is not only the practitioner who often fails to 
clearly segregate the circulatory, vasomotor, and trophic phenomena, but 
even in recent contributions of special investigators no dearth of misconcep¬ 
tions can be found. 

Perhaps it is the intricacy of the physiological, anatomical, and patho¬ 
logical data on the one hand, and the misconstruction or misinterpretation of 
the perplexing objective signs on the other, that account for the lack of 
general comprehension. 

It seemed appropriate at this juncture, therefore, to assemble, analyze, 
and critically interpret the maze and multitude of facts bearing on these 
subjects, and now at our disposal. And this with a view to establishing a 
correct approach and a clearer insight into both diagnosis and modes of 
therapy in the fields under consideration. 

But the usual text-book treatment of the subject matter would, it appears 
to the author, hardly suffice to give that fundamental knowledge upon which 
an understanding of the many varied manifestations can be built up. And 
so, to accomplish the purpose in view, it seemed not unwise to leave the 
beaten paths and to diverge and intrude with intent at considerable length 
into allied departments of anatomy and physiology. If, by conducting the 
reader through all those related, basic, and essential facts that only extensive 
research into many fields of the literature can disclose, the work of personal 
investigation be minimized and confined to the perusal of but one volume; and 
if, by & well chosen and well directed series of discussions the burden of com¬ 
prehension be facilitated, the work herein incorporated will not have been in 
vain. 

Although the greatest importance has been accorded the pathology and 
clinical manifestations of the organic vascular affections- in which domain 
the author’s experience has been ample to elucidate many of the mooted 
points—it was deemed wise to give more extensive consideration to the 
conclusions of others in some of the fields. And so, for the exposition of 
the normal circulation of the extremities, of thrombosis, of the vegetative 


VI 


PREFACE 


nervous system, and of the vasomotor neuroses, the views of a number 
of excellent authors have been more thoroughly incorporated. To the 
important researches of such investigators as Beneke, Aschoff, Cassirer, 
Hering, Muller, Dresel, Langley and others must be given credit for much 
that is of fundamental importance. Since their works may be inaccessible 
to many American readers, their essential deductions and conclusions have 
occasionally been given in extenso. 

It is a pleasure to give acknowledgement to Miss Caroline Kleppner and 
Mrs. Harry Friedman for their excellent assistance in the researches on 
thrombo-angiitis obliterans; and to accord credit to my secretaries, Miss 
Ida Lipnitz and Miss Natalie Wood for help in the preparation of the manu¬ 
script. Thanks are due to the W. B. Saunders Company for their valuable 
cooperation in the publication of this volume. 

Leo Buerger. 

iooo Park Avenue, New York City, 

May , 1924. 


CONTENTS 


CHAPTER I 

Introduction. z 

CHAPTER II 

Anatomical Considerations. 3 

CHAPTER III 

The Minute Structure of the Vessels .n 

The Capillaries.. 

The Arterioles and Venules.. 

The Arteries.^ 

CHAPTER IV 

The Vasomotor Nervous System.22 

CHAPTER V 

Functions of the Vasomotor Nervous Mechanism . . CC . ' ..36 

CHAPTER VI 

Physiology of the Peripheral Circulation.48 

CHAPTER VII 

Physiology of the Capillaries.57 

CHAPTER VIII 

Methods of Investigating Capillary Circulation.63 

CHAPTER IX 

General Circulation under Pathological Conditions.69 

CHAPTER X 

Local Circulation.71 

Local Anemia or Ischemia.71 

Hyperemia. 73 

CHAPTER XI 

Functional Disturbances of Peripheral Circulation.76 

The Superficial Circulation in Obstructive Vascular Diseases.80 

CHAPTER XII 

Collateral Circulation.82 

CHAPTER XIII 

Circulation in the Extremities Under Pathological Conditions.87 

CHAPTER XIV 

The Trophic Functions of the Nervous System.90 

CHAPTER XV 

Trophic Disorders of the Skin.96 

CHAPTER XVI 

General Considerations of Thrombosis.100 

























Vlll 


CONTENTS 


Page 

CHAPTER XVII 

The Forces Engaged in Thrombus Formation. 102 

CHAPTER XVIII 

Physical Explanations of Thrombosis. io 5 

CHAPTER XIX 

Mechanical Types of Thrombosis .m 

CHAPTER XX 

Thrombosis of Chemical Origin.118 

CHAPTER XXI 

General Causes of Thrombosis.123 

CHAPTER XXII 

Gangrene—General Considerations.127 

CHAPTER XXIII 

Methods of Investigation of Gangrene.130 

CHAPTER XXIV 

Diagnostic Symptoms—Arterial Pulsation.132 

CHAPTER XXV 

Diagnostic Symptoms—Pain.135 

CHAPTER XXVI 

Diagnostic Symptoms—Intermittent Claudication.137 

Symptoms.137 

Historical. 139 

Clinical Types.140 

Dysbasia Angiosclerotica Intermittens.140 

Functional Vasomotor Type (Oppenheim).142 

Intermittent Claudication in Other Territories.146 

“Acute Forms” of Intermittent Claudication.148 

Apokamnosis (Goldflam) or Artificial Intermittent Claudication.151 

Pathology.*.151 

Critical Summary.154 

Explanation of Phenomena.155 

Differential Diagnosis. 157 

CHAPTER XXVII 

Forms of Gangrene.157 

CHAPTER XXVIII 

Classification of Gangrene .x6o 

CHAPTER XXIX 

Clinical Examination in Gangrene.162 

CHAPTER XXX 

Traumatic Gangrene .x68 

CHAPTER XXXI 

Thermic Gangrene. I72 

CHAPTER XXXII 

Gangrene Due to Chemicals and Drugs. *. .xSx 

CHAPTER XXXIII 

Microbic Gangrene. 187 































CONTENTS 


IX 


CHAPTER XXXIV 

Microbic Gangrene (Continued).• 190 

Gas Gangrene. ig 0 

CHAPTER XXXV 

Gangrene Complicating Infectious Diseases.203 

CHAPTER XXXVI 

Injuries to the Blood Vessels and Gangrene.204 

CHAPTER XXXVII 

Aneurysms.208 

CHAPTER XXXVIII 

Treatment of Injuries to the Blood Vessels.209 

CHAPTER XXXIX 

ThROMBO-ANGIITIS OBLITERANS—INTRODUCTION.213 

CHAPTER XL 

Thrombo-angiitis Obliterans—General Clinical Concept.214 

CHAPTER XLI 

Thrombo-angiitis Obliterans—Acute Stage.218 

CHAPTER XLI I 

Thrombo-angiitis Obliterans—Chronic Stage.219 

CHAPTER XLIII 

Thrombo-angiitis Obliterans—Clinical Picture.231 

CHAPTER XLIV 

Thrombo-angiitis Obliterans—Appearance of the Limb.235 

CHAPTER XLV 

Thrombo-angiitis Obliterans—Ischemia.. . 237 

Mechanical or Hydrostatic Ischemia. 237 

Vasomotor Ischemia in Thrombo-angiitis Obliterans.240 

CHAPTER XLVI 

Thrombo-angiitis Obliterans—Erythromelia.242 

CHAPTER XLVII 

Thrombo-angiitis Obliterans—Cyanosis.250 

CHAPTER XLVIII 

Thrombo-angiitis Obliterans—Edema. 254 

CHAPTER XLIX 

it . rf 

Thrombo-angiitis Obliterans—Intermittent Claudication.255 

CHAPTER L 

Thrombo-angiitis Obliterans—Pain.258 

CHAPTER LI 

Thrombo-angiitis Obliterans—Coldness.261 

CHAPTER LII 

Thrombo-angiitis Obliterans—Arterial Pulsation.263 
























X 


CONTENTS 


Page 

CHAPTER LIII 

Thrombo-angiitis Obliterans—Mental Symptoms.270 

CHAPTER LIV 

Thrombo-angiitis Obliterans—Vasomotor Symptoms.271 

CHAPTER LV 

Thrombo-angiitis Obliterans—Osseous Changes.275 

CHAPTER LVI 

Thrombo-angiitis Obliterans—Statistical Data.276 

CHAPTER LVII 

Thrombo-angiitis Obliterans—Etiology.277 

CHAPTER LVIII 

Thrombo-angiitis Obliterans—Migrating Phlebitis.279 

Thrombo-phlebitis without Symptoms.280 

Thrombo-phlebitis with Symptoms of Limited Vein Involvement.280 

Migrating Phlebitis Causing the Patient to Seek Treatment.281 

Both Migrating Phlebitis and Thrombo-angiitis Play Equally Important Roles 

in the Symptom-complex.284 

Migrating Phlebitis or Thrombo-phlebitis Involving Both Upper and Lower 

Extremities.286 

Extensive Fulminating Migrating Phlebitis.291 

Cases in Which Absolute Evidences of Deep Arterial Involvement Are Lacking . 291 
Conclusions from Vein Lesions. 292 

CHAPTER LIX 

Thrombo-angiitis Obliterans Involvement of the Upper Extremities.294 

CHAPTER LX 

Thrombo-angiitis Obliterans—Associated Arteriosclerosis.306 

CHAPTER LXI 

Thrombo-angiitis Obliterans—Pathology.307 

CHAPTER LXII 

Thrombo-angiitis Obliterans—More Detailed Histopathology.321 

CHAPTER LXIII 

Thrombo-angiitis Obliterans—Pathology in Lethal Cases.368 

CHAPTER LXIV 

Thrombo-angiitis Obliterans—Diagnosis.374 

CHAPTER LXV 

Thrombo-angiitis Obliterans—Treatment.378 

Prophylactic Treatment.379 

Conservative Treatment.380 

Operative Treatment.382 

The Selection of Therapeutic Procedures.384 

CHAPTER LXVI 

Athero- or Arteriosclerotic Disease—Clinical Manifestations.385 

CHAPTER LXVII 

Arteriosclerosis—Pathology.394 

CHAPTER LXVIII 

Arteriosclerosis—Minute Pathology. . ..402 





























CONTENTS 


xi 


CHAPTER LXIX 

Arteriosclerosis with Thrombosis—Clinical Course 

CHAPTER LXX 

Arteriosclerotic Gangrene with Diabetes 

CHAPTER LXXI 

Arteriosclerosis—Diagnosis. 

CHAPTER LXXII 


Arteriosclerosis—Prognosis.. . 

CHAPTER LXXIII 
Arteriosclerosis—Treatment. 

CHAPTER LXXIV 

Miscellaneous Affections of the Arteries. . . 

CHAPTER LXXV 
Hypertrophy of the Arteries. 

CHAPTER LXXVI 
Acute Arteritis. 

CHAPTER LXXVII 
Tuberculosis of the Arteries. 

CHAPTER LXXVIII 
Syphilitic Arteritis and Gangrene. 

CHAPTER LXXIX 
Periarteritis Nodosa. 

CHAPTER LXXX 

Syphilitic Disease of the Veins. 

CHAPTER LXXXI 

Migrating Phlebitis—Miscellaneous Varieties . . 


CHAPTER LXXXII 
Vascular Occlusion of Doubtful Origin. 


Mal Perforant 


CHAPTER LXXXIII 


CHAPTER LXXXIV 

Embolism and Thrombosis. 

Arterial Obturation without Immediate Symptoms. 

Embolic and Thrombotic Gangrene after Infectious Diseases. 

CHAPTER LXXXV 

Embolic Gangrene—(Continued) . . .. 

Embolic Gangrene with Cardiac Disease. 

Post-operative Embolic or Thrombotic Gangrene. 

Thrombotic Gangrene in Healthy or but Slightly Diseased Vessels. 

CHAPTER LXXXVI 

The Vasomotor and Trophic Neuroses—General Considerations. 


Page 

421 

427 

431 

434 

435 

445 

447 

448 

455 

45d 

462 

464 

470 

472 

474 

479 

480 

481 

485 

485 

489 

490 

499 
























Xll 


CONTENTS 


Page 

CHAPTER LXXXVII 

The Skin and the Vegetative Nervous System. 5°4 

CHAPTER LXXXVIII 

Diagnosis and Localization of Vegetative Nerve Lesions. 5°9 

CHAPTER LXXXIX 

Vasomotor and Trophic Disturbances in Lesions of the Central Nervous 

System. 5*3 

CHAPTER XC 

Neurotrophic Disorders in Spina Bifida.514 

CHAPTER XCI 

Vasomotor and Trophic Disorders in Peripheral Nerve Lesions.518 

CHAPTER XCII 

Neuroses and the Periarterial Sympathetic Nerves.521 

CHAPTER XCIII 

Traumatic Vasomotor Spasm.. 523 

CHAPTER XCIV 

Local Shock.526 

CHAPTER XCV 

Chronic Acroasphyxia.527 

CHAPTER XCVI 

ErYTHROMEL ALGIA. 53I 

CHAPTER XCVII 

The Acroparesthesize.537 

CHAPTER XCVIII 

Gangrene Without Organic Vascular Disease.539 

CHAPTER XCIX 

Raynaud’s Disease.542 

CHAPTER C 

Scleroderma. 559 

CHAPTER Cl 

Multiple Neurotic Gangrene.567 

CHAPTER CII 

Vasomotor Instability.570 

CHAPTER CIII 

Atypical Vasomotor Neuroses.572 

CHAPTER CIV 

Clinically Borderline Cases.• • • 575 

CHAPTER CV 

Treatment of Vasomotor Neuroses.57^ 





















CONTENTS xiii 

Page 

CHAPTER CVI 

Capillary Microscopy. 584 

CHAPTER CVII 

Capillary Microscopy in the Vasomotor Neuroses. 590 

CHAPTER CVIII 

Capillary Microscopy in Special Forms of Vasomotor Disease. 598 


Bibliographic Index. 603 

Index of Subjects. 609 












THE CIRCULATORY AFFECTIONS OF THE 
EXTREMITIES INCLUDING GANGRENE, 
VASOMOTOR AND TROPHIC 
DISORDERS 


CHAPTER I 

INTRODUCTION 

The subject of the vascular affections and gangrene of the extremities 
will receive consideration together, because of the intimate and inseparable 
clinical bonds that link these affections together. It is by virtue of the multi¬ 
plicity of causal modalities that may bring forth similar or identical phe¬ 
nomena, and through the overlapping of manifestations of varied origin, that 
intricate clinical complexes are produced. We know that gangrene may be 
the issue of wholly different pathologic processes resulting from the action of 
direct or indirect mechanical, thermal, and chemical agencies, and a variety 
of organic vascular disorders as well as through almost inexplicable neuro¬ 
genic derangements. Many of the prodromal phenomena of diseases of 
wholly diverse genesis may so closely resemble each other as to produce 
perplexing and clinically confusing pictures. It is because of these facts, 
that a discussion of the ultimate and most destructive lesions of 
varied motivation must needs be considered in connection with, and in rela¬ 
tion to all others that may, even though only occasionally, bring about a 
similar issue. Only through such a grouping and comparative study 
can the clinician obtain a correct appreciation, either of the origin of the 
phenomena themselves, or of the proper classification and recognition of the 
diseases in question. 

We need but pause for a moment to reflect on the intricacy of that maze 
of factors upon which the clinical features of vascular disturbances depend, to 
realize that not only is a knowledge of the modus operandi of each and of 
every one of them essential, but a critical balanced judgment is necessary for 
purposes of clinical diagnosis. Whilst for the recognition of a valvular 
lesion or an area of pulmonary consolidation, relatively few fundamental 
anatomic, acoustic and pathologic facts are necessary, the conditions upon 
which the manifestations of organic vascular and vasomotor disease of the 
extremities depend, are exceedingly complex. Even with a thorough knowl¬ 
edge of the distribution of the vessels, their gross and minute morphology, 
their roles as dispensers of blood, their means of substituting by-paths 
through existing anastomoses; and even with a thorough acquaintance with 
the pumping mechanism, we are not thoroughly equipped for a compre¬ 
hensive, critical and analytical approach to the subject. Although the 

i 1 


2 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


physiologists of the past have given us an abundance of conclusions, these 
have been modified and amplified by recent investigators, yielding a multi¬ 
tude of facts. A thorough comprehension of these is a prerequisite for cor¬ 
rect explanation of the many varied clinical manifestations. 

Whilst it is relatively easy to arrive at a clear concept of the objective 
effects of mechanical and hydrostatic forces, the heart action, the patency of 
the vascular channels, and the abridgement or intensification of these forces 
through gravity action, there are still others of imponderable nature that are 
clinically known to be at work, and that have been experimentally proven 
capable of exerting an influence. Let us recall merely a few of these. The 
vasomotor mechanism with its reflex play of function, its dependency on 
external circumstances and even on emotional states, is capable of evoking 
clinical pictures of obscure nature; even more so when the two diverse factors, 
the mechanical or hydrostatic and the neurogenic are acting in conjunction, 
independently, associated or related, as the case may be. In the light of 
recent investigations of inherent capillary activities, a new vascular domain 
has loomed up as capable of participating in the clinical vascular complexes. 
For not only is the neuromuscular mechanism governing the arterioles and 
venules recognized, but to the capillaries is relegated a function of their own 
and one susceptible to varied impressions. Whilst the mechanical and hydro¬ 
static factors may find a response in dilatation or constriction of capillaries 
when there is pressure, a plenum, or a void; and whilst a certain control 
(usually constrictive) of the vegetative system is not denied, local metabolic or 
chemical influences may bring forth a functional reply in the form of dilata¬ 
tion of corresponding capillary areas. 

We have then in the mechanical, hydrostatic, nervous and autonomic 
capillary forces, a combination of patrly passive, partly actively function¬ 
ating links, that may intrude upon the clinical picture and make it complex 
and hard to interpret. 

The author has, therefore, included in his treatise, not only the vascular 
affections that may evoke trophic and destructive tissue changes, but also 
those nerve or vasomotor maladies that occasionally or often call forth similar 
clinical symptoms. 

To properly comprehend all phases of this subject, we believe that our 
preparatory knowledge should include a study of the following: 

i. The anatomy and histology of the normal vascular apparatus of the 
extremities; 


2. The anatomy and physiology of the nervous mechanism that controls 
the vessels; 

3. A consideration of normal and pathological local circulation; 

4. A comprehension of the origin and action of thrombosis, of mechanical 
and of thermal agencies on the tissues; 

5. The subject of gangrene in relation to its clinical diagnostic and patho¬ 
logical aspects; and 

6. An exposition of the clinical course of all those diseases of either 
organic vascular, neurovascular or vasomotor causation, that have, and still 
do give the physician much difficulty in clinical differentiation. 

Although all of these topics will be discussed, their clinical, pathological 
and diagnostic phases will receive the more comprehensive consideration. 


ANA TOM I CAL CONSIDERA TIONS 


3 


CHAPTER II 


ANATOMICAL CONSIDERATIONS 


In applying anatomical data to the interpretation of the circulatory affec¬ 
tions of the extremities, the course, distribution, and anastomoses of the 
vessels interest us from certain special angles. What may be germane to the 
fundamental hypotheses and observations of the anatomist and embryologist, 
is of importance only in an elementary way. For a clarification of our con¬ 
cepts of the organic and neurogenic vascular maladies, we are more particu¬ 
larly concerned with the following phases of the anatomy. 

1. The topographical relations of the vessels to the body surface; and 

2. The normal anastomoses, and therewith the foundation for collateral 
blood supply. 



r, t>njorum 


Scalenus anter. 
u. thyreoideit 
inferior 
*»**'■ rente, 
medium 

gland, thyreeidea 
tr. thy rear rvicaliS 

a. vtrtcbraUs 

a rnamnmna ini . 
7 hryngms infer. 


thyrenidea infer, 
tt. titrduivas 
median 
a. wroth 


vena thy tea idea 


Fig. i. —Course of the axillary artery and its branches. ( Sobotta) 

Diagnosis of the circulatory affections of the arteries of the extremities 
will be greatly facilitated through an accurate knowledge of the surface 
topography of the important arterial trunks supplying the peripheral parts. 
In order to refresh the student’s memory, the essential facts necessary for 
the recognition of obliterated peripheral pulses will be given here. Whilst 
it may be easy to diagnosticate the exact points of blockage of the axillary or 
brachial arterv by palpation alone, the patency of the larger arteries of the 






4 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

lower extremities may be indeterminable by reason of their inaccessibility to 

the examining finger. r 

The Axillary Artery (A. Axillaris) (Fig. i).—This is a continuation or 
the subclavian in its course through the axillary space. Beginning at the 
lower border of the first rib, in the apex of the axillary space, it courses along 
the outer wall of the space to the lower border of the teres major, where it 
is known as the brachial artery. 



Fig. 2.—Course of the brachial artery. ( Sobotta) 

A line drawn from the middle of the clavicle to a point mid-way between 
the two condyles at the humerus with the arm abducted at right angles indi¬ 
cates its course. It may be digitally compressed in its lower or third portion 
(below the pectoralis minor) against the humerus just within the edge of the 











A NA TOM I CAL CONSIDERA TIONS 


5 


coraco-brachialis and biceps. The pulsation of the axillary artery is not 
usually visible. In very thin individuals and in some persons after exertion 
especially if arteriosclerotic, the pulse may become evident with the arm lifted 
vertically. Palpation along the coraco-brachialis muscle in the lower part of 
its course just under the pectoralis minor will usually reveal the pulsation. 

The axillary vein occupies a more superficial position and is situated toward the ulnar 
(posterior) side, being neither visible nor palpable under normal conditions. 

The brachial artery (Fig. 2) is a prolongation of the axillary, beginning 
at the lower border of the teres major, and terminating just below the bend 
of the elbow where it divides into the radial and ulnar arteries. Above, 
the vessel passes along the inner side of the arm, but lower down it is deflected 
somewhat outward, so that in its lower part it is on the anterior surface of 
the brachium. 

A line drawn from the junction of the outer and middle thirds of the folds 
of the axilla when continued to a point mid-way between the condyles of 
the humerus, indicates its course. In its upper two-thirds it can be felt easily 
and compressed against the inner side of the humerus in an outward and 
slightly internal direction along the internal border of the coraco-brachialis 
and biceps. It may pass either just along the border of this muscle or be 
overlapped by the inner edge of the biceps. At the middle of the arm it 
is also easily palpated and compressed. In the lowest third if pressure is 
applied backwards, it will direct it against the brachialis anticus as the latter 
lies over (in front of) the humerus. 

For diagnostic purposes it should be remembered that the palpating 
finger should be directed laterally against the humerus, along the inner border 
of the biceps, whilst above the elbow the palpating finger must be directed 
backward. 

With the forearm flexed at right angles and with the biceps relaxed the 
brachial pulse can be traced downward to within a short distance above the 
bend of the elbow, where compression backwards against the brachialis 
anticus will usually allow the plantar aspect of the fingers to detect the artery. 
In finding it, slight lateral displacement of the mesial border of the biceps 
with the tips of the palpating fingers may be necessary. 

The Radial and Ulnar Arteries.—The point of bifurcation of the radial 
and ulnar arteries is usually so deeply situated that it is difficult to palpate 
the pulses in this situation, and therefore an imperceptible beat is of little 
clinical value. 

The ulnar artery arises just below the bend of the elbow and passes first distally and 
inward beneath the muscles which arise from the internal condyle of the humerus and at 
the junction of the upper and middle thirds of the forearm, taking a more vertical direction. 
At the wrist it passes over the anterior annular ligament to the radial side of the pisiform 
bone and then courses across the palmar surface of the hand forming the superficial palmar 
arch. Three parts have been described, an antibrachial portion extending to the upper 
border of the anterior annular ligament; a carpal portion resting on the annular ligament; 
and lastly, the palmar portion. 

The lowermost portion of the antibrachial course of the ulnar artery as it 
lies on the flexor profundus digitorum with the tendon of the flexor sublimus 
digitorum toward the radial side is usually the site of an ulnar pulsation. 

Anomalies, however, occur that account for absence of pulsation in this region, such as 
those instances in which the ulnar artery is represented only by muscular branches, the 
vessel being substituted by a persistent median or interosseous artery. On the other 
hand the ulnar artery may be more superficial, passing down the forearm over, instead of 
under, the muscles arising from the internal condyle. Such a course may also be followed 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


when the artery has a normal origin, and occasionally it passes to the ulnar ^rderoi the 
forearm between the palmaris longus and the flexor sublimus digitorum (Cunningham). 


The radial artery is also only palpable in its lower part between the tendon 
of the brachio-radialis and that of the flexor carpi radialis. Here it is very 
superficial, and on dissection is brought into view as soon as the fascia is 

The usual radial pulse may be absent when the artery passes to the dorsal 
surface of the arm much higher up than usual, and in such cases the super- 



Fig. 3.— The popliteal space, with the popliteal vessels. ( Sobotta ) 

ficial volar branch also has its origin at a higher level, and passes downward 
to the usual situation of the radial. In such instances it is represented by a 
very slender vessel, may give a very small pulse and be erroneously inter¬ 
preted as indicating diminished pulsation in a radial artery. 

The femoral artery is best felt just below the interior edge of Poupart’s 
ligament, where the vessel can be compressed against the brim of the pelvis, 
just outside of the ilio-pectineal eminence. Somewhat below this it is 
separated from the femur by more muscle. At the apex of Scarpa’s triangle 
it is more difficult to palpate, and the direction of pressure must be outward 
and somewhat backward in order to displace it against the femur. In the 
most accessible portion of its course just below Poupart’s ligament, only slight 









A NA TOMICAL CONSIDERA TIONS 


7 


pressure of the finger is necessary to elicit a femoral pulse. As the pulse is 
traced downward, however, when a point 3 or 4 finger breadths lower is 
reached, more pressure is required for its detection. The normal femoral 
vein is neither palpable nor visible. 




•"* ; s, ; /(tops ft “HU v-i 


Tibiaiis posterior 


/ lexer dipitorum 
lon pus 


n. perotuirns 1 
(<otriiittirti\) 
tibialis % 
1 enu paphtru 


turns pop!itens 
m. sold 
tendo in. 
plantaris 


art. tibialis 
posterior 


Gastroc¬ 
nemius X 


lim its tibialis 
rami miisintarcs 


lip. ladniatiuu 
tendo ealt tinni.' 


a. peronant 


/ Uxor fmltun 
loti pus 


resitmealnm 
peronaeoruM 
super/u > 


tendo ealeamvs 


.vtt'ii Mir aha 


remit pophtear 


neryii- tibialis 


vasa tihiiilia 
posteriora 


Perouarus longits 
PeroiHieiis Imris 


lip. Inciniatnin 


, retiiiitenltiiii 
p> 7 •< ma ear. stip< > 


uert'ii s t Unit/is 


vena paphtru 

n un $tophrmt 
/wrva 

'aput Infertile 

■nrornetnd 


art. poplitea 


caput media!, 
(iustiocncmu 

j 'asit surtfiin 


u. «cun safe riot 


n . fie ron (tens 
communis 


rami tmtsai- 
lare< nervi 
tibia Hi 


a. poplitea 


Soleus 


uerrns tibialis 


art. tibialis 
posterior 


Plantaris 


Soleus 


are genu 
inferior 
media Us 


Figs. 4 and 5.—Popliteal vessels and their branches at the knee posteriorly and in the leg 

( Sobotta) 

The popliteal artery (Fig. 3) should be palpated with the patient lying in 
a prone position, 1 and with the leg flexed, but relaxed at right angles. Its 

1 See p. 133. 

























8 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

course through the popliteal space must be remembered; its relations bemg 
internal to the internal popliteal nerve, and with the vein external and behind 
(that is, nearer the surface of the popliteal space). The popliteal artery is a 
continuation of the femoral, extending from the termination of the latter 




a.poplitea 


ml. grim 
V///W, /ill. 
art. genu 
infer. luterali 


'He.! 


nrhire 


1(10/1(1(1/s. 


flexor 

digitonnu 

lotigns 




J ibid!is 
anterior 


it. peronaeus 
profundus 

temio in. 
tibiaiis anteriorly 


fig. 

- miewtum 


n. peronaeus 
profu mi a ' 

art. dorsali* 
.//> . 


art. 

tibialis poster, 
tendo 

in. tibialis I 
postcrioris 


a. malieolaris 
post, luediaiis 
Undo nt. flexor is 
lulllmis iongi ■ 


m i nis tibialis 

temio m. pimttnris 


or.', recur/tu*. 
tibiuh * poster 


fixtensor digit, 
long, x 


a. tibialis 
anterior 


art . 

gean irt f r 
me t fiat Is 


IMpliteus' 


Solen s x 


Tibialis 

posterior 


r. calcaneus 
medial is • 


I’eromiens , 
long us X 

1 1 .nen. tongas x 

a recut reus tibialis ants 
. n. peeo/uien^pro/undni 

*. peronaeus '•itperfte. 
Penmaens hnigtts * 

arti ria tibialis, 
anterior 


I'eivimcus longns 


f lexor haUucis 
longas 


‘eronoens brevis 

mil us aamtiun icons 


rete ea/eaiiriiia 


art. tibialis- 
anterior 


nemts peronaeus 
superfiaalis x 


!fronaeus brevis 

Extensor hallueis longas 
/ v tensor digit, longns 

ramus prrforans 
art. peronaeae 
rete rnaUeolare 
tolerate 


art. malieolaris 
ant. lateralis 


tendo in. peronaei III 


extensor digitontm 
brevis 


<uterine metalarseae 
dorsates 


a. tibialis 


a. malieolaris 
post, lateralis 


tendo calcaneus 

romits cn/etweus 
lateralis 


arl. poonaitt 


Figs. 6 and 7. On the left the popliteal artery dividing into the anterior and the pos¬ 
terior tibials, giving off peroneal artery; on the right the course of the anterior tibial 
artery. ( Sobolta ) 

at the adductor magnus, to the lower border of the popliteus muscle, divid¬ 
ing there into the anterior and posterior tibial arteries. 

\\ here it is not possible to palpate the arteries in stout individuals, a 
popliteal pulsation can be occasionally demonstrated as follows: the limb on 















A NA TOM I CAL CONSIDERA TIONS 


9 


the side to be examined is allowed to hang over the other in such a manner 
that the popliteal space is supported by the patella of ihe other leg. Then 
the tip of the foot of the superimposed limb may show a transmitted motion 
synchronous with the beat of the compressed artery. 



Fig. 8 . —Course of the dorsalis pedis artery and its branches. ( Sobotla ) 


A reference to Fig. 3 will demonstrate the relation of the popliteal artery 
as it takes an almost vertical direction through the popliteal space, the vein 
and nerve. It should be palpated just as it emerges from under the semi¬ 
membranosus muscle in the upper part of the rhomboid. 

The posterior tibial artery (Figs. 4, 5 and 6) is a continuation of the 
popliteal, beginning at the bifurcation of the latter at the lower border of 






CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the popliteus muscle and coursing downward to the groove between the 
internal malleolus and os calcis, where it divides into the internal and external 

1 Except for that small portion that lies immediately above the ankle, it 
lies very deep, being separated from the tibia by the muscles of the calf. 
Pulsation is perceptible only in its lower portion at the inner side of the an e, 
where it lies under the deep fascia between the flexor longus digitorum and 
tibialis posticus tendon behind the internal malleolus. The artery can often 
be seen to beat between the internal malleolus of the tibia, and the mesial 

margin of the Achilles tendon. , 

The anterior tibial artery (Fig. 7) constitutes the other branch of the 
popliteal, beginning at the lower border of the popliteus muscle, passing 
directly forward between the tibia and fibula, over the upper border of the 
interosseous membrane. Then it lies in front of the latter, coursing downward 
to the ankle joint where it becomes the dorsalis pedis artery. 

It is inaccessible to palpation except in its lowermost portion, where 
occasionally pulsation can be felt. Just lateral to the external border of 
the extensor propreus hallucis as the latter crosses the vessel obliquely, and 
between this and the extensor longus digitorum it becomes more superficial. 
Here and below this point, with the foot flexed and the extensors relaxed, 
some 2 inches or more of the artery frequently give a distinctly perceptible 
pulsation. This pulse, however, is not a constant phenomenon and for clini¬ 
cal purposes the beat in the dorsalis pedis is of much greater diagnostic 
significance. 

The dorsalis pedis artery is a continuation of the anterior tibial artery 
downward to the proximal portion of the first intermetatarsal space (Fig. 8). 


The artery lies just lateral to the extensor longus hallucis tendon between the latter and 
the mesial portion of the extensor digitorum, but closer to the former. The artery is best 
palpated in the region of the proximal portion of the first intermetatarsal space just lateral 
to the tendon of the extensor longus hallucis. If we employ the plantar aspect of the 
tips of 3 or 4 fingers and allow these to palpate along a line projected vertically upwards 
from the interspace between the great and second toes along the lateral margin of the 
extensor longus hallucis tendon, the normal pulsating artery will rarely escape the finger 
as it lies over the middle cuneiform bone. Not infrequently, particularly in moderately 
arteriosclerotic individuals, a visible pulse can be detected. 


The Normal Anastomoses.—From a study of these, conclusions may be 
drawn as to the possible functional responses through existing channels, 
whenever one of the following modes of impediment obtain; namely, limited 
vascular blockage (embolic), ascending or centrally directed obturation, 
embolic closure with ascending and descending blockage (progressive throm¬ 
boses), and localized or diffuse coarctation of the vascular lumina (athero¬ 
sclerosis, endarteritis obliterans). 

A more complete exposition of this subject will be found in the chapter 
dealing with Collateral Circulation (Chap. XII) and the diagnostic signifi¬ 
cance of the anastomoses will be dealt with in the discussions of the various 
arterial diseases. 


THE MINUTE STRUCTURE OF THE VESSELS 


IT 


CHAPTER III 

THE MINUTE STRUCTURE OF THE VESSELS 

THE CAPILLARIES 

Simple endothelial tubes or capillaries consist of cells or elongated lanceo¬ 
late plates with oval nuclei united by narrow lines of cement substance. 
Traced from the arteriole there is a gradual transition, the beginning of the 
capillaries being recognized by the final disappearance of nuclei cells. By 
virtue of a network of such channels distributed throughout the tissues, 
there is provided an excellent mode of insuring the passage of the blood in 
intimate contact with the tissue elements. 

A nerve distribution along and surrounding them has been recognized; and 
while contacts between these fiber-endings and the endothelial cells have not 
as yet been brought to light, it is fair to assume that such junctions do indeed 
occur. A direct nerve supply can, therefore, be predicated for the vascular 
capillaries. 

The endothelial layer of cells which constitutes the capillary when con¬ 
tinued into the arteries and veins, forms the innermost layer of the intima 
lining these vessels. Tissue structures which differentiate the vascular areas 
are laid down upon this endothelium. The essential difference between the 
larger arteries and veins is found in the relative thickness of their walls. In 
the arteries smooth muscle predominates. In the veins, although a suffi¬ 
ciency of smooth muscle exists, there is a preponderance of white and yellow 
elastic tissue and the walls are not as thick. 

Recent researches by Vimtrup (1922) have confirmed the existence of 
the contractile cells first found by Rouget (1873) in the walls of the capil¬ 
laries. Mayer had described similar cells subsequently (1902), although 
his observations were accorded little credence. 

Investigations of the activity of the capillaries of the frog’s tongue (Vim¬ 
trup) led to the histologic demonstration of a meshwork of contractile cells. 
With suitable fixation and staining methods certain nuclei distinctly differ¬ 
ent from ordinary endothelial nuclei were discovered. 

Krogh states that the form of these nuclei varies with the state of contraction of the 
capillary. On a dilated capillary they are broad and very thin; by contraction they become 
narrower and thicker, their cross-section approaching the form of a circle. The proto¬ 
plasm belonging to these nuclei can be made visible by suitable staining, but even then it 
requires high-power immersion lenses and—especially on dilated capillaries—a good 
light, preferably excentric, to see it in its entirety. 

On a dilated capillary the protoplasm surrounds the nucleus as a continuous layer 
on the capillary wall, but it diminishes in thickness towards the periphery, which is very 
irregular and sends out a number of very fine branches along and especially around the 
capillary wall. The branches show at their base a definitely triangular cross-section, but 
soon become flat. Sometimes they become broader and divide, but the ends are always 
very thin and pointed. Most of the branches lie athwart the capillary and are of such 
length that they reach those from the other side. Some of the branches, however, run 
along the capillary, and both the protoplasm and the nucleus are, as a rule, stretched in 
this direction. 

There can be no doubt that the richly ramified muscle cells on the capillary wall are 
the same as those originally found by Rouget in the hyaloid membrane. 

The above data warrant the conclusion (Krogh) that the capillary walls, 
too, consist of an endothelial tube and external muscular coat; and that 
the essential difference between capillaries and larger vessels is to be found 
in the arrangement of the muscle. In the former the musculature is repre- 


12 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


sented by a wide-meshed network through which the greater part of the 
endothelium is free to transfer substances with a minimum of resistance; 
whereas in the larger arteries and veins a continuous layer of muscle is 
present. Even the muscular coat of the capillaries has a definite tonus 
subject to nervous, hormonal and other influences. 

THE ARTERIOLES AND VENULES 

The arterioles are situated between the arteries proper and the capillaries, 
and between the capillaries and the veins proper lie the venules. Some 
authors distinguish between an arterial and a venous capillary. Although 
structurally alike, one may differentiate these on a functional basis. Capil¬ 
laries vary in size, but they are structurally uniform in character. The terms 
“arterial” and “venous” in this connection imply a change in character of 
the contained blood. No distinct point in the capillary net can be recognized 
at which such a change occurs. 



Fig. 9. —Schematic representation of the relation of the muscle cells and connective tissue 
about the arterioles and venules. (Hooker and Sabin) 

Towards the periphery and along the arteries, there is a gradual decrease 
in the size of the lumen and in the thickness of the vessel wall. This attenu¬ 
ation goes hand in hand with the diminution in connective tissue elements. 
The smallest arteries are composed of an endothelial lining (intima), a layer 
of connective tissue fibers and a layer of muscle fibers. In the arteriole 
there occurs an elimination of the connective tissue layer between the endo¬ 
thelium and the muscle fibers. The arteriole is, therefore, made up of muscle 
and endothelium alone. Towards the periphery, the arterioles subdivide and 
become diminutive; with this, the muscular layer is attenuated gradually 
until but the simple endothelial capillary tube is left. 

The capillaries in their turn give way to the venules, a transition that is 
accomplished by the addition of a connective tissue layer. This antedates 
the inclusion of muscle fibers. Thus there is a sharp structural contrast 
between the arteriole and the venule. The arteriole is characterized by the 
muscle substance intimately overlying the endothelial tube, while the venule 
exhibits connective tissue in the same situation (Sabin). 

This morphologic distinction is depicted in Fig. 9 where the differential 
structural disposition of muscle cells about the arterioles, and of connective 
tissue on the venules is evident. 




THE MINUTE STRUCTURE OF THE VESSELS 


13 


THE ARTERIES 

Arteries of medium size offer rather typical pictures in exemplification of 
the muscular variety and may be briefly described here. 

In cross section the intima has a folded appearance directly applied to the 
plication of the internal elastic membrane. The latter presents a striking 
corrugated line marking the external limit of the inner coat. The endothelial 
cells are so thin that they are recognizable mainly as projecting nuclei. But 
between the endothelium and the elastic membrane there is a fine layer of 
connective tissue and elastic fibrils. 

The media is composed of circularly distributed muscle fibers interspersed 
with elastic tissue plates, whose presence can be intensified and brought to 
view by appropriate elastic tissue stains. The external elastic membrane, 
the middle and external tunics, are separated by a distinct layer. 

The adventitia is of varying thickness and is relatively larger in 
the medium sized arteries than in the larger ones. It is composed of fibrous 
tissue and elastic fibers, contains the vaso-vasorum, and main lymph channels 
of the vessel wall. 

The Structure of the Arteries in Embryonal Development.—Two types of 
arteries have been distinguished, the elastic and the muscular types. Of the 


Fig. 



I0 .—Transverse section of the aorta of an embryo (about the middle of embryonal 
life); numerous elastic fibers in the media; none in the adventitia. ( Aschoff) 


former the aorta is an example, of the latter, the arteries of the. extremities— 
such as the brachial. For a correct understanding of what is normal and 
what constitutes atherosclerotic or arteriosclerotic change, the normal alter¬ 
ations in the arteries through embryonal life and during the first 2 or 3 months 
of extrauterine life must b e borne in mind. 

About the fourth month in both types of vessels differentiation in the 
intima, media and adventitia occurs, with simultaneous development of 
muscle fibers, elastic tissue and fibrillar connective tissue. 

The Elastic Type .—The aorta (Fig. 10) as an example, in. the fourth 
month of the embryo presents an intima made up of endothelium, a rela¬ 
tively broad elastica interna with rather regular folds. The media includes 
about ten rows of nuclei, containing numerous elastic lamellae interspersed 






14 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

between these. Towards the adventitia these are absent, although no 
distinct membrane demarcating the boundary can be discerned. Here the 
adventitia is broader than the media, and made up of connective tissue. 




Fig. ii.—T ransverse section of the aorta of an embryo taken at the end of embryonal life. 

{Aschoff) 


Aav. 


.ext. 


El.int. 

End* 

Fig. 12 .—Section of the brachial artery of an embryo taken at the end of embryonal life. 

( Aschoff ) 

The muscular type of artery, as the brachial at 6 months, has a well 
developed endothelial layer and elastica interna. The media contains 
muscle cells arranged in a more orderly fashion with a very few interspersed 


























THE MINUTE STRUCTURE OF THE VESSELS 


15 


elastic fibers. The adventitia and the media are distinctly separated 
through an elastic membrane. The adventitia is different being char¬ 
acterized by the appearance of two laminae, the inner one disposed longi¬ 
tudinally, the external more or less circularly and irregularly. Further¬ 
more, longitudinally coursing elastic fibers in the inner portion of the adventi¬ 
tia appear at this stage in a rather characteristic fashion, for such a layer is 
absent in the elastic type of vessel. 

The Arteries Shortly before Birth. —Late in the embryonal stage the 
differences between the muscular and elastic types are more striking. In 
the aorta, besides the general enlargement, the absence of plication is a 
feature. In the media the marked development of the elastic membrane is 
prominent, the muscle cells being relatively few in number. The elastica 
externa is here also absent. The adventitia becomes relatively narrow, 
being made up of connective tissue without elastic elements (Fig. n). 

In the brachial artery (muscular type) the internal elastic membrane 
becomes thicker, being regularly folded on section (Fig. 12). In the media 
the muscle cells are prominent in number and spindle shaped, particularly in 
the outer layers. The elastic fibers have multiplied in the media, although not 
so intensively as in the musculature. In the adventitia, however, the elastic 
fibers have hypertrophied and are disposed in a longitudinal direction, being 
in far greater abundance here than in the media. The separation from the 
media through the elastica externa here, too, is noteworthy. 

In short, the differences in and during the embryonal development of the 
two types of vessels are: The appearance here and there of connective tissue 
layers in the intima of the vessels of the elastic type with marked development 
of the elastic membrane; in the arteries of the muscular type, the media and 
musculature are prominent, as are also the elastica externa and the longi¬ 
tudinal elastic fibers of the adventitia. 

The Arteries in Extrauterine Development. The Elastic Type .—Three 
layers in the intima have been described in the elastic arteries of children 1 
(Fig. 13). On cross section the elastica interna is seen to be split into two 
or three lamellae, that frequently reunite. Here and there, are interrup¬ 
tions that probably indicate openings in the lamellae. Adjacent and on 
the inner side are numerous longitudinal elastic fibers, including a similar 
distribution of cells. Then there is a circular layer of elastic fibers and 
finally an innermost delicate layer of connective tissue, upon which the 
endothelial cells are deposited. Jores has called that layer, which lies 
against the elastica interna, an elastic muscular layer, the next one of hyper¬ 
plastic thickening of the intima, and the innermost, the connective tissue 
layer. 

The growth and development of the musculo-elastic (as well as the hyper¬ 
plastic layers) attain their maximum at the climax of bodily development, 
namely between the twenty-fifth and thirtieth years. The connective tissue 
coat develops more tardily, possibly after the thirtieth year. These three 
layers may attain considerable thickness at an age when morbid changes in 
the vascular system are not as yet to be expected. It is only when the hyper¬ 
plasia becomes extensive (especially of the connective tissue coat) that the 
so-called sclerotic process is said to begin. 

For our studies of the peripheral circulation we are concerned especially 
with the following type. 

The Muscular Type .—Characteristic for these arteries in their further 
development, is the relative marked hypertrophy of the muscular layer 
1 Aschoff, Description given as applying to ages of 1-4 years. 


16 


CIRCULATORY AFFECTIONS OF TIIE EXTREMITIES 



Fig. 13. —Cross section of the aorta of a child 3 years of age; in the intima three layers, 
the external cut transversely being a musculo-elastic longitudinal layer; the middle portion 
a hypertrophic elastic layer; the innermost one of very delicate connective tissue belonging 
to the normal period of growth. ( Aschoff ) 



Fig. 14. Cross section of the radial artery at the climax of its development (third 
decade); slight development of a hypertrophic elastic coat in the intima, belonging to the 
normal period of growth. ( Aschoff ) 











































THE MINUTE STRUCTURE OF THE VESSELS 


17 



Fig. 15. —Normal posterior tibial artery and vein in cross section. Here there is but the 
slightest degree of thickening of the intima in places. 


Fig. 



16.—Normal posterior tibial artery; muscular type (high power). 


2 






18 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


(Fig. 14). As far as the adventitia is concerned, it is believed that the longi¬ 
tudinal elastic fibers undergo a marked increase during the early years. On 
the other hand the inner elastic layers do not develop that marked differen¬ 
tiation and increase that are noticeable in the larger arteries of the elastic 
type (the aorta and carotid). The hyperplastic intimal layer may be slight 
in extent, but the musculo-elastic longitudinal layer is absent or but little 
marked. In the adventitia, on the other hand, the elastic fibers are 
exceedingly prominent. 



Fig. 17.—A, Elastic tissue stain of a normal (posterior tibial) artery showing early 
thickening of the intima (possibly early arteriosclerotic thickening) with reduplication 
of the intimal elastic fibers; IEL, internal elastic lamina; M, muscular coat (media); 
A, adventitia; P, perivascular fatty connective tissue. 

Figs. 15 and 16 illustrate a “normal” posterior tibial artery and vein. 
For purposes of orientation and comparison with the lesions to be described 
in later chapters, it may be well to point out the following characteristics; 
the adventitia is narrow and loosely bound with the surrounding connective 
tissue as well as with accompanying veins; the circular muscular layer is 
relatively well developed (media) and evidences great dearth of vascular 
elements; the intima is narrow except in those zones of slight thickening that 
may be regarded as within the normal, or insufficient to be designated as 
arteriosclerotic. Thickening of the intima within the physiological limits is 
depicted in Fig. 17. 

A somewhat more marked example of the effects of hydrostatic and 
mechanical (perhaps also toxic) stresses on the development of the periph¬ 
eral arteries is depicted in the sections taken from the dorsalis pedis artery 
of an adult. In Fig. 18 we have an excellent illustration of the relation of 
the artery to the veins, the absence of vascularization of adventitia and media 
so characteristic of the normal. In the discussion of the inflammatory 






THE MINUTE STRUCTURE OF THE VESSELS 


19 


diseases of the arteries (arteritis, periarteritis and thrombo-angiitis, etc.) and 
of the intravascular thrombotic processes, it will be seen how penetration of 
these coats with new formed vessels may occur; and how in some of them, the 
adventitia and the relation of the artery to its accompanying veins becomes 
altered. 

In the section of the artery, too, when seen under greater magnification 
(Fig. iq), the hypertrophy of the middle coat is in evidence. Slight prolifer¬ 
ative changes in the intima, also, mark the transition of a normal artery into 
the early stages of arteriosclerosis. 



Fig. i8 .—Low power transverse section of almost normal dorsalis pedis artery and veins, 
showing slight hypertrophy of the media and beginning thickening of the intima; the avas¬ 
cular condition of the media and adventitia are well shown, and the loose connection 
between artery and veins. 


The Senile Changes in the Arteries. —Aschoff, Marchand, Jores and 
others point out that the first senile changes are the hypertrophy of the 
musculo-elastic longitudinal layers of the intima (Eigr— 2q). There is no 
sharp differentiation between the antecedent normal development and the 
subsequent pathological thickening. It is only the proliferating connective 
tissue that signalizes a distinct senile change. This connective tissue is 
deposited between the elastic fibers of the hyperplastic layer, occupying 
there a dominant position. Besides, it is laid down as a strong connective 
tissue lamella upon the old intima. It is often difficult to differentiate 
between normal physiological thickening and senile sclerosis. In the aorta 


20 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


and larger vessels there is usually associated fatty degeneration. Jores 
believes that this process begins in the outermost layers of the intima, that 
is, in the musculo-elastic longitudinal coat (Fig. 21). Later fatty degenera¬ 
tion and calcification may take place; and coincidentally or subsequently 
reactive and degenerative processes in the new-formed intimal layers, with 
thrombotic deposits in the lumen and organization. 



Fig. 19.—Cross section of slightly hypertrophic dorsalis pedis artery showing slight 
intima hypertrophy. The intima is somewhat thicker than normal, but avascular; adven¬ 
titia normal (higher magnification of Fig. 18). 


In the elastic type of arteries (aorta) the changes in the media are less 
intensive. Atrophy does occur and elastic lamellae and muscle fibers dis¬ 
appear. Although microscopically evidenced, the macroscopic destruction 
of the media is relatively slight. Streak-like areas of fatty degeneration in 
the middle coat and very fine lime deposits do appear. 

In the arteries of the extremities (muscular type) the change in the media 
and the calcification are noteworthy, and preponderate over the initimal 
changes. When the arteries of this type in the extremities undergo calcific 




THE MINUTE STRUCTURE OF THE VESSELS 


21 


alterations, the earlier manifestations thereof will be represented by fatty 
degeneration especially pronounced in the media; the lime deposits follow 
-(figure). Bone formation as a sequel is not uncommon. 



Fig. 20. —Cross section of the aorta at the time of complete development (third decade); 
in the intima still distinct division into three layers, but with hypertrophy of the connective 
tissue. ( Aschoff) 

The intimal lesions in the peripheral vessels are also of importance and 
are essentially represented by the endarterial thickening through connective 
tissue proliferation. Fatty degeneration is not so characteristic here. 
According to Monckeberg the changes in the media of the arteries of the 
extremities preponderate numerically over those in the intima. 


Mea. 


Fig. 2i. —Transverse section of the aorta with beginning atherosclerosis at the end of 
the fourth decade; marked connective tissue hypertrophy and fatty degeneration of all 
three parts of the intima. White areas are those of fatty degeneration. ( Aschoff ) 

The Development of the Arteries and Their Subsequent Pathological 
Changes. —It is rather interesting to observe that those elements of the 
arteries that exhibit their most profound development late in embryonal 
life, and in the early years of extrauterine growth, also suffer the greatest 
pathologic alterations in atherosclerosis. If the latter be regarded as a 
disease of deterioration, functional stresses (or overactivity) must partici- 










































22 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

pate in the resultant lesions. So in the larger arteries of the elastic type, by 
virtue of the arterial pressure and its constant variations and the pulsative 
forces, extensive and distensive stresses must needs exert longitudinal and 
lateral tension on the elastic element of the intimal tubes. With this comes a 
tendency to tearing in the longitudinal, as well as in the circular direction. 
Such factors have been regarded as playing an important role in the conse¬ 
quent pathologic alterations. 



Fig. 22.—Transverse section of the femoral artery with beginning arteriosclerosis at the 
end of the fourth decade; in the media areas of calcification. ( Aschoff ) 


In explanation of the precocious development of atherosclerosis the ques¬ 
tion has been raised as to what influence toxic elements ( e.g . alcohol, 
nicotin) may have upon the elastic elements of the arteries; or what role 
an acquired predisposition on the part of the elastic elements through pre¬ 
vious infectious diseases may play. In the muscular type of vessels the 
muscle fibers would necessarily suffer greater strain through the arterial 
pulsations and excessive dilatation and contraction. Changes in blood 
pressure and in the blood stream too, have been regarded as of importance. 
The special demands of overacting musculatures of the extremities; the 
functional demands of the peripheral arteries; the increased tension result¬ 
ing from difficulties in the capillary flow; the modifications due to vasomotor 
influences—all these are believed to be motivating elements. 


CHAPTER IV 

THE VASOMOTOR NERVOUS SYSTEM 

It is a perplexing but nevertheless an interesting clinical fact that many 
of the objective symptoms resulting from organic closure of the larger 
arteries and veins of the extremities can be easily confused with manifesta¬ 
tions of altogether different etiologic significance. These are in the main 
nutritive and trophic derangements on the one hand, and circulatory and 
vasomotor on the other hand. And, therefore, it behooves the clinical 
observer to be able to discriminate between atrophies or lesions of the skin, 
and other tissues that result from circulatory impairment (purely trophic or 
nutritive), and similar alterations due altogether to nerve influences (neuro¬ 
trophic). And so, too, disturbances in the vasomotor mechanism may cause 



THE VASOMOTOR NERVOUS SYSTEM 


23 


phenomena simulating closely those of hydrostatic and mechanical vascular 
origin. 

A loose concept obtained by a cursory reading of text books on neurology 
concerning neurotic trophic lesions should be supplanted by a systematic and 
detailed study of the anatomy and physiology of the sympathetic system, 
and what is known concerning the neurotrophic, and neurosecretory paths. 
For the sake of completeness, therefore, the salient features of the anatomy 
and physiology of this portion of the nervous system are described 
in detail. 

Course of Vegetative Nerve Fibers. —The cerebrospinal motor fibers that 
enter the sympathetic system end in branches about the sympathetic cells, 
but never directly in vessel walls or other peripheral localities. Their course 
is of varied length, some terminating in the nearest ganglion cells- in the cor¬ 
responding ganglion of the ganglionic cord, others traversing several ganglia; 
still others continuing until they reach the most peripherally situated ganglia. 
It is most probable that all sympathetic cells are influenced through motor 
fibers emanating from the cord; on the other hand, the motor ganglionic 
fibers of the sympathetic, never act upon other ganglionic cells. Even 
these fibers are of different length ending at points near or far from their 
source. 

Medullated fibers originate in the central nervous system with their cells 
in the gray substance, travel in a cerebral or spinal nerve, or with several of 
these in a cord to a sympathetic ganglion. This preganglionic cerebro¬ 
spinal fiber ends in a ganglion in that its dendrites surround the sympathetic 
cell in a dense network or in sparser distributions. The sympathetic cell 
in many instances sends a non-medullated axis cylinder to the peripheral 
tissues (the postganglionic fibers of Langley) where this terminates without 
cellular interposition. The central precellular fibers never come into contact 
with the peripheral tissues , but influence only the cells of the sympathetic system. 
So also, a sympathetic, post-cellular fiber does not connect directly with a 
ganglion cell, but is in immediate communication with peripheral tissues, 
muscles, glands or intestine. A precellular fiber may traverse one or several 
ganglia before terminating. 

The vegetative system may be subdivided into subordinate portions 
whose origins lie in various segments of the cerebrospinal axis. Five 
territories are recognized; first, centers in the corpus striatum; second, in the 
mid-brain; third, in the medulla; fourth, in the dorsal region up to the second 
and third lumbar segments; and fifth, in the region from the second to the 
fourth sacral segments (Eig^-23):" The- centers in the corpus striatum 
more recently recognized are shown in Fig. 24. 

The mid-brain, bulbar and sacral systems are not infrequently spoken of 
as belonging to the autonomic or parasympathetic system, in contradistinction 
to the dorso-lumbar portion, called the sympathetic system. 


It has been found that nicotin has a selective action on those ganglion cells in which an 
anatomical interruption of continuity takes place, with functional relaying of nerve impulses. 
Intravenous injection of nicotin as well as local application on a ganglionic node, cause 
transitory excitation followed by paralysis of the ganglion cells that lie in the relay station. 
Before nicotinization, stimulation of a fiber of the vegetative system produces a certain 
irritative effect, irrespective of whether this excitation takes place before or beyond its 
entrance into the ganglion. Nicotin paralyzes the interpolated cell only, as that irrita¬ 
tion of the preganglionic fibers is without effect; but the post-ganglionic fibers will respond 
as usual. This action of nicotin is confined to the vegetative system. The nicotin method, 
therefore, has been employed experimentally to indentify impulses that belong in the 


24 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



SpUVJ0-)V9(K8 
puv s/assaa 
snoduvyno oj; 














































































THE VASOMOTOR NERVOUS SYSTEM 


25 


vegetative nervous system. It also permits us to decide as to whether a certain ganglionic 
node is an interrupting station for certain nerve fibers. 


The sympathetic system , is composed of those spinal centers that lie in 
the lateral horns of the spinal cord, of the anterior roots emanating from these 
and leading to the ganglionic cord through the rami communicantes albi 

ffig. 25) - 

Certain cells at the point of transition between anterior and posterior horns, sometimes 
designated lateral horns or intermedio-lateral tract have been regarded as the site of 
origin of the fibers leading to the gangliated cord. Jacobsohn 1 distinguishes a nucleus 
sympatheticus lateralis superior extending from the eighth cervical to the third lumbar seg¬ 
ment, and providing all the sources of the rami communicantes of the gangliated cord. In 
the parasympathetic system he describes a nucleus sympatheticus lateralis inferior from the 
second sacral segment to the coccygeal; also a nucleus sympatheticus medialis inferior located 
in the fourth lumbar segment and fusing with the above in the coccygeal region. All of 
these nuclei show interruptions in continuity throughout the various segments. 

These rami are split up about the ganglia lying alongside the vertebral 
column. Here, the ganglia and their communicating fibers constitute the 
gangliated cord. The gray rami have their source in these ganglia, whence 
they course either independently (as in the case of the splanchnic nerve), or 
join the spinal nerve. The sympathetic system in a narrow sense is 
composed, therefore, of the spinal centers, the rami communicantes, the 
vertebral ganglia, the gangliated cord of the sympathetic and the peripheral 
sympathetic nerves. The upper limit of this system is the first thoracic nerve, 
and, in man, it extends downward, to the second or third lumbar segment. 
It is noteworthy that there are no sympathetic fibers arising from the cervical 
portion of the cord. In the cervical region, the gangliated cord has 3 ganglia; 
in the thoracic n to 12; in the lumbar 4 to 5, and in the pelvic 4 to 5 sacral 
and 1 a coccygeal ganglion. The afferent fibers passing through the rami 
albi <to the gangliated cord, arise from widely separated spinal segments. The 
efferent fibers, that is, the post cellular fibers are in rather close proximity, 
since in their further course they follow closely the spinal nerves in the imme¬ 
diate vicinity. 

The superior cervical ganglion supplies the vessels and part of the 
glandular apparatus of the head, and part of the vessels of the brain, the 
dilator of the iris and Muller’s muscle of the orbit. The stellate ganglion sends 
fibers to the thoracic viscera, and accelerating fibers to the heart. The rest 
of the gangliated cord supplies the muscles of the vessels of the extremities of 
the trunk, the muscles and glands of the skin, and the blood vessel muscles 
of the intestinal tract, of the lungs and intestines. 

The anterior extremities receive their vasomotor fibers through 
the anterior roots from the 4th to the 10th dorsal nerves. According to 
Bayliss the vasoconstrictor nerves of the upper extremities leave the spinal 
cord in the anterior roots from the 3rd to the nth thoracic nerves, whilst 
those for the posterior extremities are found in the nth, 12th and 13th 
thoracic, and 1st to 3rd lumbar roots, in animals. The skin of the trunk in 
man derives its vasomotor nerves from the anterior roots of the dorsal and 
lumbar nerves. The lower extremities receive supply from the anterior roots 
of the last three thoracic and upper three lumbar nerves. It was formerly 
believed that only arteries received vasomotor fibers. It has been shown 
more recently, however, that the veins are also thus supplied. 

jacobsohn, Abhandl. d. k. preuss. Akad. d. Wissensch., 1908. 




26 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 24.—Reflex connections in the vegetative nervous system. Transference of an 
impulse at I into Auerbach’s plexus; II, to the postganglionic sympathetic cell in the para¬ 
vertebral ganglion; III, to the preganglionic sympathetic cell in the cord; IV, to the pre¬ 
ganglionic parasympathetic cell in the medulla; V, to the vegetative cell in the corpus 
striatum. ( Modified, after Dresel) 












THE VASOMOTOR NERVOUS SYSTEM 


27 



Fig. 25. —Schematic drawing of the sympathetic nervous system. The dotted lines 
indicate the bulbar and spinal paths. The preganglionic fibers are seen joining the gray 
matter of the cord and the ganglia. The solid lines (to subclavian artery and piloerectors) 
indicate postganglionic fibers. ( Muller ) 




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^(cmc/u/a pen. 


Ssmemss um 

onterece 


IF.Crrtvea&egmtnt. 

















28 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Parasympathetic System .—We need merely to refer to this in a general way 
here, and point out to what extent this part of the vegetative nervous 
system deals with vasomotor impulses. The parasympathetic system is 
composed of the cranial and the sacral autonomic systems. Over the 
posterior roots of all of the dorsal and the upper lumbar segments there 
travel impulses, which serve to bring about vasodilatation and inhibition of 
perspiration in the territory of the trunk and the extremities. 


That portion of this system, which is called the cranial autonomic system, does, not 
concern us here, for its main portions constitute the oculomotor nerve, and ganglion ciliare, 
and the vagus. The sacral autonomic system is not involved in the innervation of the 
vessels of the extremity, but communicates with the pelvic plexuses, the nervi pelvici, and 
innervates the genitals and bladder (nervi erigentes). 


But there is one portion of the parasympathetic system, which is said to 
furnish vasodilator fibers, and sweat inhibiting paths for the trunks and the 
extremities. The dorsal and upper lumbar spinal segments (Muller) not 
only give origin to sympathetic fibers for the vasoconstrictors, for the secre¬ 
tion of sweat and the pilomotors, but antagonistic impulses also travel 
herein. The parasympathetic system is included in the posterior roots and 
not in the anterior. Our knowledge of its functions, however, is not based 
upon morphologic data; relevant histologic imformation is not at hand, nor 
has the point of origin of these paths in the gray matter of the spinal cord 
been discovered. 

Cerebral Vasomotor Centers. —Daily observations teach us that blood 
vessels are influenced by psychic states and therefore, by way of the cerebrum. 
The pallor of the face after fright, the blush after joy or erotic ideas are 
examples. 

Cortical cerebral vasomotor centers for the various peripheral nerves were 
experimentally sought but without convincing results. ~ Even the vasomotor 
disturbances after cerebral lesions, such as hemorrhage and tumors, and the 
vasomotor manifestations after cerebral injury are too little characteristic and 
uniform to allow of binding conclusions as to localization. There are no 
certain data at hand to prove the existence of special vasomotor centers in 
the cortex. In a search for such centers elsewhere in the brain, physiological 
experiments have brought to light that vegetative functions may indeed be 
influenced from a very small cerebral territory. It is believed that the cere¬ 
bral vasomotor center resides in the mid-brain, in the optic thalamus and in 
the gray matter of the third ventricle. 

The removal of the cerebrum in a dog is not followed by any permanent functional 
vascular derangement. There are, however, localities in other portions of the brain that 
may be shown to affect the vasomotor nerves. Studies on hyperthermia have demon¬ 
strated that special modes of stimulating the corpus striatum lead to elevation of tempera¬ 
ture (“heat puncture” of the German authors). So also, ablation of the anterior and 
mid-brain of rabbits destroys the function of heat regulation, while exclusion of the anterior 
brain alone is not followed by this result. 1 Karplus and Kreidl demonstrated that a center 
for vasomotor innervation lies in the mid-brain, especially in the gray matter of the third 
ventricle. Not only are vasomotor phenomena dependent upon psychic changes and 
emotion, as manifested by external cutaneous phenomena, but distribution of blood in the 
organs of the chest and abdomen is affected thereby. Different parts of the body are not 
equally influenced by emotional states. The blood in the extremities seems to be dimin¬ 
ished during intellectual work, with simultaneous increase of the blood content in the brain 
and abdominal organs. 

1 Isensch-Krehl, Arch. f. exp£r. Path. u. Pharmakol., Bd. 70. 


THE VASOMOTOR NERVOUS SYSTEM 


29 


Although the general tone of the vessels may be influenced through a 
circumscribed area in the third ventricle, it is a mooted question as to whether 
all vessel innervation has the same origin. Fluctuations in the tonus are not 
dependent on impulses traveling from the spinal cord or cerebral nerves in a 
centripetal direction alone. Activities in the neencephalon and excitation 
of the ganglion cells of the mid-brain following irritant effects of the blood 
itself, may also be effective. 

In short, the region of the mid-brain, the optic thalamus, and the gray 
matter of the third ventricle, contain a v center or centers from which sensory 
impulses are transferred to the vasomotor paths. This center admittedly 
controls the general tone of vegetative innervation and also the special reac¬ 
tions of the vessels. The fluctuations in tone of the centers are subject to 
and related to stimuli from three sources; firstly, through the spinal cord and 
centripetal cerebral paths; secondly, through psychic mutations jin the cere¬ 
brum; and thirdly, by direct excitation of the ganglion cells in the mid-brain 
through special irritants in the blood. 

According to Starling there is a small region of the medulla oblongata on each side of the 
mid-line in the neighborhood of the facial nuclues, that sends impulses. The normal 
impulses travel down the cord as far as the dorsal region, and then pass outward by the 
dorsal and upper lumbar nerves. These facts have been adduced from experimental 
section of the cord at various levels. A marked fall in blood pressure follows division on 
a level with the origin of the nrst dorsal nerve. Destruction of the above mentioned area 
in the medulla also causes immediate lowering of the blood pressure. These conclusions 
are further confirmed by the fact that, whereas stimulation of the anterior roots of the 
cervical and lower lumbar and sacral nerves has no influence on blood pressure, a rise of 
the latter can be obtained by stimulating any of the anterior roots from the first or second 
dorsal to the second or third lumbar. 1 That portion of the medulla concerned with the 
sending out of the tonic vasoconstrictor impulses, is spoken of as the vasomotor center. 
Here it is subject to and receives stimuli from all portions of the body, from the higher 
centers of the brain and especially from the viscera of the chest and abdomen through the 
vagi. And so, the sum of the impulses arriving at the center produces a state of average 
continued activity which is responsible for the maintenance of arterial tone and for the 
regulation of the arterial blood pressure. 

Furthermore, paralysis of the vasomotors of the body, as manifested by dilatation of all 
the vessels of the trunk and extremities, follows section through the medulla oblongata or 
cervical cord, while this does not occur with an interruption made above the medulla and 
just below the corpora quadrigemina. Glaser rather doubts the existence of such a vaso¬ 
motor center; but he is in accord with the view, that the vasomotor innervation travels 
through paths from the mid-brain through the medulla. Centers of limited function— 
local vasomotor centers—controlling the vessels of the brain, the salivary glands or the 
dilators of the facial skin territory, may according to this author reside in the medulla. 

A few clinical observations corroborate the physiological deductions 
regarding the existence of chief vasomotor centers. A beautiful example of 
vasomotor disturbances induced by central lesions is the case of Rossolimo. 2 

A man 38 years of age had manifestations pointing to a growth in the right motor zone; 
namely, clonic contractions of the left side of the body and headaches; the left hand was 
cyanotic, edematous, and his temperature diminished. Operation disclosed a cyst, which 
was followed by a disappearance of the vasomotor manifestations. From this it was 
concluded by the author that the cortical vasomotor center lies near the motor area. 

Oppenheim distinguishes a vasomotor form of Jacksonian epilepsy, and a 
vasomotor monoplegia, in which there are attacks of vasomotor disturbances 
in the arm and face of one side, with or without loss of consciousness, and 

1 Starling, E. H., Principles of Human Physiology, Phila., 1915. 

2 Rossolimo, Deutsch. Ztschr. f. Nervenh., 6, 1895, p. 76. 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


persistent vasomotor symptoms in the same territory, with only slight 

paresis and atrophy. . . 

So also vasomotor changes with cyanosis are observed with the common 
forms of hemiplegia, with edema of the paralyzed side, symptoms that are 
not altogether to be explained by lack of function. . 

Subcortical vasomotor centers have been referred to the optic thalamus. 

Little is known regarding vasodilator centers in the human. The. cere¬ 
brum doubtless has an activating influence on the dilators, as evidenced in the 
vascular changes in the integument of the face. 

From the center in the medulla oblongata the conducting paths ol the 
vasomotor system pass to the lateral tract of the cord. Kocher in his stuck 
of vasomotor palsy after traumatic lesions of the vertebral column and cord, 
observed dilatation of the vessels and elevation of temperature of the 
paralyzed extremities. Such vasomotor phenomona, however, . usually 
disappeared. In some cases pallor and diminution in temperature initiated 
the symptoms, these being irritative symptoms or evidences of incomplete 
paralysis of the vasomotors. Compression of the cord by tumors has been 
observed with vasomotor symptoms. 

Recent Views on Anatomy— While the descriptions that have preceded 
represent the accepted views prevailing for the last io years, a school of 
Continental investigators (Kraus, Brugsch and Dresel) has arisen that voices 
somewhat different anatomic as well as physiologic concepts. 

According to Dresel there is a superior center of the vegetative nervous 
system in the corpus striatum. Subordinate to this there is a subthalamic 
center in the mid-brain which is in communication with the corpus striatum 
through the bundle of Forell and through the tinea lenticularis (“Linsenkern- 
schlinge”)- Nerves pass from the mid-brain to all points of origin of sympa¬ 
thetic and parasympathetic fibers in the mid-brain, medulla, thoraco-lumbar 
and sacral segments of the spinal cord. Whilst, according to Langley, only 
the thoraco-lumbar cord contains sources of origin for the sympathethic, 
and whilst parasympathetic fibers emanate from the other parts of the cord 
and medulla, it has been shown more recently that at least in the case of the 
dorsal vagus nucleus, both parasympathetic and sympathetic ganglion cells 
coexist (Brugsch, Dresel and F. H. Lewy). Furthermore, such a combina¬ 
tion is believed to be possible in other parts of the central nervous system. 


These parasympathetic and sympathetic nerves arising from the central nervous system, 
course in the following structures; in the ocular motor nerve, the corda tympani, the vagus, 
the white rami communicates, the gangliated cord, and in the nervus pelvicus, in the form of 
preganglionic, mostly medullated fibers. They pass to a second group of ganglion cells, 
namely the ganglion ciliare, ganglion submaxillare, the ganglia of the gangliated cord, the 
paravertebral ganglia and in the so-called enteric system. In the latter groups of cells, the 
interruption of all vegetative peripheral fibers takes place. 

Parasympathetic and sympathetic fibers course as postganglionic fibers to their termi¬ 
nations. Most organs contain both parasympathetic as well as sympathetic fibers. 
According to Dresel the so-called enteric system 1 of Langley (which the latter regarded as 
an independent plexus, especially in the heart and in the intestinal tract) should more 
properly be included in the total mass of post-ganglionic cells; and this because it has been 
shown that these cells signify for the vagus (both anatomically and functionally) the very 
same thing that the cells of the ganglionic cord do for the sympathetic. Therefore, the 
following scheme has been suggested by this author. 2 


1 Ganglion cell groups in the walls of viscera. 

2 This scheme has been obtained through the kindness of K. Dresel (Berlin) in a personal 
communication; to be published in Handbuch d. Med. Kraus u. Brugsch., 1922. 


THE VASOMOTOR NERVOUS SYSTEM 


31 


NUCLEI IN CORPUS STRIATUM (VEGETATIVE) 
Mid-brain Nuclei (Vegetative) 

\— - -j 

Parasympathetic nuclei Sympathetic nuclei 


cranial bulba sacral para- 

parasympathetic sympathetic 

nuclei nuclei 


Preganglionic parasympathetic 
fibers 


Ganglionic cells of the post-ganglionic 
parasympathetic fibers (ganglia ciliare 
submaxillary, etc., plexus parasympa¬ 
thetic, post-ganglionic myenteric, 
enteric systems). 


bulb, sympa- thoraco- 

thetic nucleus lumbar 

symp. nuclei 

I_ I 


Preganglionic sympathetic 
fibers 


Gangliated cord Paravert. ganglia 


Postganglionic fibers 

I I 

End-organs 


Spinal Vasomotor Centers.—There is no doubt but that there are seg¬ 
mentary centers for vessel innervation in the spinal cord. After a transverse 
lesion of the spinal cord, vasomotor responses are possible in the anaesthetic 
lower parts of the body. Reflex patchy rubor follows in the cutaneous area 
that is irritated with mechanical stimuli, such as needle pricks, provided that 
the corresponding spinal cord segment is intact. 

Stimuli arising by way of the blood may also excite the spinal vascular 
centers. In asphyxia, even after section of the cord, an active vasocon¬ 
striction in the paralyzed part of the body is noted. This response is not 
obtainable if the spinal cord is destroyed. 

The lateral horns are believed to contain the ganglion cell groups for 
vegetative function; and more correctly, in the intermediary zones between 
the anterior and posterior horns, where pyramidal or comma shaped ganglion 
cells control these functions. The cervical cord contains no such cells up to 
its lowermost portion. From the eighth cervical segment up to the lumbar, 
we find the lateral sympathetic nucleus. From this region emanate the vaso¬ 
constrictors for the face, the upper extremities, the trunk and the lower 
extremities. From the lateral and inferior mesial sympathetic nucleus 
that extends from the lowermost part of the lumbar cord into the sacral, 
the vascular nerves for the lower part of the intestines and for the inner and 
outer genitalia have their origin. The ganglion cells of the intermedio- 
lateral tract are aggregated into large groups in the middle and lower sacral 
cord. These completely fill the transitional zone between the anterior and 
posterior horns. Since the vasomotor nerves for the genitals, namely the 
nervus erigens or pelvic nerve arise from this segment, the conclusion is 
warranted that these cell groups are related to the vascular innervation of the 
sexual organs. It is impossible to differentiate, however, the cells that 
influence vascular innervation, and those which control the musculature of 
the pilo-erectors or the sweat glands. In syringomyelia and poliomyelitis 
vasomotor disturbances occur, such as vascular palsy, and lividity attri¬ 
butable to disease of the gray substance. 













32 CIRCULATORY AFFECTIONS OF TIIE EXTREMITIES 


Vasomotor Paths in the Spinal Cord. —We still lack proof of the existence 
of special paths of conduction for the excitation of the vegetative functions. 
Clinical and experimental experiences warrant the conclusion that vasomotor 
impulses traversing each half of the spinal cord may arrive at both parts of 
the body. This explains the relative paucity of the vasmotor paralytic 
symptoms in the Brown-Sequard lesions. It has not as yet been proven that 
vasomotor paths course in the lateral tracts. The dominating vasomotor 
center in the mid-brain seems to conserve and regulate the general vascular 
tone. Perhaps qualitative alterations occur in the centers as the result of 
varied influences, and through these manifold reactions of the spinal centers 
ensue. It is not even definitely shown that the tonus is dependent upon 
the existence of certain paths, and the substantia gelatinosa or even the gray 
substance has been suggested as possible vehicle for the impulses. Some 
suggest that emotions may cause certain changes in the biotonus or in the 
general nervous excitability, because of the varied responses in depressive 
and sanguine states. 

This tonus which controls the spinal cord is under the influence not only 
of the emotions, but also of sensory impulses. Various reflexes in the vegeta¬ 
tive system, such as dilatation of the pupils or contraction of the tunica dartos 
follow severe pain impulses. In explanation of these phenomena it has been 
pointed out that all sensory paths cannot be in direct communication with all 
the vegetative centers in the spinal cord, or the medulla and mid-brain. 
Therefore, it may be accepted that impulses of sensory or of other nature 
may cause an alteration in the excitability of the gray substance of the spinal 
cord, with changes in its tonus. The latter in its turn influences the vaso¬ 
motor cell groups. 

In all probability the dominant tone of the spinal vasomotor centers is not transmitted 
through isolated paths, but propagated through the whole gray matter, and is modified 
through a multiplicity of influences, pain, temperature and the like. 

The importance of the dominating vascular center in the brain and of the tonus influ¬ 
ences that emanate therefrom, is shown in the experimental work on the effect of section of 
the cord on the heat regulating center. The latter is disturbed in proportion to the heighth of 
the spinal cord section, and depending upon the number of spinal centers that are thereby 
excluded from the influences of the cranial vasomotor center. High section of the cord in 
animals makes heat regulation impossible, and the animals die. Therefore, above the 
cervical cord there is a regulating center (vasomotor) that controls the tone of the inferior 
centers, but the manner of conduction has not as yet been discovered. 

Relations of Spinal and Sympathetic Systems .—It must be remembered that 
all the paths between the spinal cord, ganglionic cord and peripheral nerves 
have not been definitely established. A reference to Fig. 26 will show the 
course of the known fibers in continuous lines, of the hypothetical fibers, in 
dotted lines. 

The medullated fibers crossing from the cord into the sympathetic system arrive in the 
lateral horns; from here they pass through the anterior roots, into the peripheral nerves, 
making a sharp curve through the rami communicantes. Here they are medullated and 
constitute the ramus communicans albus. When the fibers arrive in the proximally situ¬ 
ated ganglion of the sympathetic cord, they come into contact with the ganglion cells in 
parts, but their greatest portion continues cephalad and caudad in the internodal portion 
either to communicate with ganglia at other levels, or to enter the cervical sympathetic 
or splanchnic. 

The non-medullated fibers course through the gray ramus to the peripheral spinal 
nerves where they supply the skin, vessels, sweat glands and piloerector muscles. How¬ 
ever, there is also a communication between the gray ramus and the spinal cord (shown in 
the diagram in a dotted line) although their course has not been definitely established. 
Some fibers also pass to the thoracic and abdominal organs. 


THE VASOMOTOR NERVOUS SYSTEM 


33 



o 

V c* 

\ V °c 
\\ 


Nervus sympaffurus 
(Harms mtemoduiLsi 

Torie '^tf^rtdir-o.L 


Fig. 26. —Scheme of the ganglionic and spinal communications of the sympathetic. 
Solid lines^indicate definitely known paths; dotted lines still hypothetical. ( Muller ) 


D.H 



Fig. 26 a .—Reflex paths in the cord. White, receptor neurones; black, connector 
neurones; dotted, excitor neurones; A, voluntary system; B, involuntary system; P.R.G., 
dorsal root ganglion; D.H., dorsal horn; L.H., lateral horn; V.H., ventral horn; Sy.G., 
sympathetic ganglion. (Gaskell and Bayliss ) 

3 























34 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The schematic drawing given by Gaskell and Bayliss (Fig. 2 6 a) shows 
the centers of the sympathetic system in the spinal cord, and the relative 
disposition of the voluntary and involuntary systems. The cells of origin 
in the lateral horn are indicated at LH in Fig. 26a. 

Antagonistic Innervation of the Vessels.—Although the finding of antago¬ 
nistic innervation in the visceral territory offers no particular difficulties, 
the relations that obtain in the case of the vessels of the extremities are 
somewhat more difficult to interpret. The rami communicantes emanating 
from the anterior roots appear to contain only the vasoconstrictor fibers. 
Clinical facts speak for the probability that vasodilator influences travel from 
the posterior horn through the posterior root, and then by way of the spinal 
ganglia into the periphery. So we can explain the active hyperemia in the 
irritated cutaneous territory, when sensory nerves undergo excitation. An 
irritative reflex erythema 1 takes place, one that is absent when the reflex arc 
is broken by section of the nerve. The vasodilator impulses appear to have 
their own fibers, and they leave the spinal cord through the posterior 
roots, and then course with the sensory fibers through the spinal ganglia to 
the periphery. 

And so it has been accepted by many that the vessels of the trunk and 
extremities are supplied by an antagonistic double innervation in which 
constrictor and dilator impulses functionate. 

Some time after electrical stimulation of the sciatic stump after section vasodilator 
changes are noted, while stimulation immediately after section results in vasoconstriction. 
From this the conclusion has been drawn, that the dilator fibers are preserved longer than 
those of vasoconstrictor function. 

According to Starling, Bayliss and others, besides the main vasomotor center in the 
medulla there is a series of subsidiary centers in the gray matter of the lateral horns of the 
cord, giving origin to the fibers that go to make up the white rami communicantes. These 
centers make possible a certain degree of adaptation between the blood supply of the various 
parts of the trunk. If the spinal cord of an animal be destroyed, the blood pressure sinks 
almost to zero, and the circulation comes to an end. The spinal centers, like the chief 
motor center, are susceptible to changes in the composition of the blood delivered to them. 
But these centers may gradually take on an automatic function, replacing that of the higher 
chief center, after the medullary center has been excluded by division of the cord just below 
the medulla, and after the blood pressure has fallen. 

Clinical observations seem to warrant the conclusion that each half of 
the spinal cord sends vasomotor impulses to both sides of the body. This 
fact explains the occurrence of such minimal vasomotor deficiency symptoms 
in the Brown-Sequard lesions. 

The Peripheral Course of the Vascular Nerves.—The vasoconstrictor 
paths are interrupted by ganglia outside of the spinal cord, just as are all the 
nerves of the vegetative system, and they leave the spinal cord through the 
anterior roots. We are interested here only with the course of the vaso¬ 
motor fibers of the extremities, which are similar in their paths to those of 
the trunk (Fig. 25). 

After union of the anterior roots with the nerve bundles emanating from 
the spinal ganglion, the fibers of the vegetative function of vessel innervation 
leave the spinal nerve through the ramus communicans albus. In the gangli- 
ated cord they make contact with multipolar cells, that give rise to the post¬ 
ganglionic or postcellular nerves. The postganglionic fibers pass through 
the rami communicantes grisei (gray rami). In their course they accom¬ 
pany the spinal sensory nerve, and particularly the sensory paths. With 
these they enter the subcutaneous tissues and the vessels of the latter. This 

1 See Chap. XLVI (Dermatographia). 


THE VASOMOTOR NERVOUS SYSTEM 35 

course applies only to the vasomotor paths of the extremities and to the skin 
of the trunk. 

In some of the larger vessels (internal carotid, aorta, and renal arteries) 
nerve bundles and ganglion cells have been found in the adventitia. Such 
nerve elements have not as yet been discovered in the vessels of the 
extremities. In view of these facts, some physiologists have concluded that 
peripheral vasomotor centers may lie in the immediate vicinity of the vessels, 
giving these an independent tone. We would then have three different 
centers, the cerebral , the spinal , and the peripheral. Possibly this third 
type plays a role in the responses due to direct excitation. 

According to some investigators nerve fibers are present in the blood vessel walls. 
Glaser speaks of a reticulum of nerve fibrils in the adventitia, demonstrable with special 
vital staining methods. In the deeper layers a network is imbedded between the adven¬ 
titia and media. Between the muscle bundles there are also fine fibrils with nodes. Such 
have only been found in the larger arteries and veins. 

In the case of the smallest vessels fine fibrils can be traced about the external walls, and 
an intraparietal network also has been recognized. 

As for the capillaries they are said to be surrounded by a fine network, there being two 
accompaning nerves with numerous anastomoses. 

According to Sabin, 2 types of nerves are found, forming plexiform nets on and in the 
walls of the larger vessels. The motor type appears to be distributed so that contact is 
made with each muscular element. This set of fibers undoubtedly evokes functional vaso¬ 
motor responses. Dogiel believes that the other type is distributed to the 3 tunic layers of 
the vessel wall, terminating in flattened end-plates or specialized structure. Such fibers 
would be of sensory variety. 

Muller and Glaser 1 describe fine nerve filaments coursing along the capillaries and 
encircling these through anastomoses. 

Since true ganglion cells of the sympathetic type have not been found in 
the deeper layers of the vessels, and none at all in the peripheral arteries, the 
assumption is warranted that vascular response may occur through direct 
action upon the musculature. Indeed, the tonus of this musculature may be 
preserved after nerve section. Inasmuch as degenerative changes after the 
exclusion of nerves have not been found in the smooth muscle, Glaser takes 
exception to the view of those who would postulate a degenerative response 
in a fashion analogous to that occurring after section of a vasomotor nerve. 

Much discussion has arisen as to the course of the reflexes in these territories. Some 
investigators believe that vascular reflexes originating in the sensory nerves must pass 
through an arc of which the spinal cord forms a link. The view of Langley, that axon 
reflexes may account for the responses, is not universally accepted. According to the latter 
author, an irritation of the skin would pass through the centripetal sensory fibers, only up 
to that point where the vasomotor paths and sensory diverge, from which the impulse 
would lead through the vasomotor fibers to the blood vessels. Such would be a peripheral 
reflex arc without interposed ganglionic cells. 2 

Some of the more recent authors lean to the supposition that the vasocon¬ 
strictor impulses travel by way of the spinal cord; the vasodilator paths, 
however, may lead to the vessels without passing through the ganglia of the 
sympathetic gangliated cord. 

Dissections made by Potts have demonstrated that, as in the arm, the 
distribution of vascular nerves in the leg is much more extensive than that 
laid down in the text-books; further, that the sympathetic supply for the 
vessels of the lower extremities reaches the main vessels at intervals along 
their course. Potts also states that the small vessels differ from the large 
ones, as a rule, in not having special nerve supply, but in obtaining their 
nerve plexuses direct from the sympathetic plexus on the parent artery. 

1 Muller, Das Vegetative Nervensystem, 1920, p. 100. 

2 See Chap. V and Kroh’s substantiation of the theory of Langley, Fig. 27 a. 


36 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Distribution about the Common Femoral Artery. The branches of the superficial and deep 
femoral arteries, and the medial and lateral circumflex vessels all derive their nerve supply 
directly or indirectly from the femoral nerve. The popliteal artery derives its supply in 
part directly from the N. tibialis, and in addition receives a branch in many cases from the 
azygos nerve. The same author states that both the main trunk of the vessel as well as 
larger arterial branches receive supply direct from the nerve trunks and not through the 
medium of a continuation of nerve plexuses from the parent arterial stem. From these 
findings it would be difficult to understand the rationale of the operation of periarterial 
sympathectomy (Leriche, Chap. CV), to be described later on. 

Summary. —The vasomotor system, therefore, is made up of a structure 
of superimposed parts, all more or less interdependent. Whilst we note in 
the nerves supplying the voluntary muscles but two divisions, we must count 
upon four or more in the vasomotor system. (Some even believe that there 
may be a vasomotor center in the cerebrum.) Vasomotor paths travel from 
here with the motor and sensory conducting system through the internal 
capsule through the subcortical large ganglia. Perhaps in the optic thalamus 
or in the caudate nucleus, interruption in their continuity takes place through 
the interposition of new cell groups. From there they are believed to pass 
further through the pons to the large vasomotor centers of the medulla ob¬ 
longata. Thence fibers pass through the lateral portion of the spinal cord to 
various levels in the latter to break up about cell groups in the middle portion 
of the gray substance, the latter being the spinal vasomotor centers. From 
these cell groups, fibers again appear that lead to the sympathetic by way of 
the rami communicantes, and from there pass further into the periphery. 
At this point in the course, namely, at the gangliated cord or somewhat 
nearer the periphery, or even in the vessel wall, further interpolation of gang¬ 
lionic cells may take place. These cells may be regarded as the most distal 
vasomotor centers. Some authors believe that an additional autonomic func¬ 
tion or capacity must be ascribed to the smooth muscle of the vessel 
musculature. 


CHAPTER V 

FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 

The Vasoconstrictor Nerves. —Experimental data corroborate the view 
oft expressed that the vasoconstrictor nerves leave the spinal cord by the 
anterior roots of the spinal nerves from the first dorsal to the third or fourth 
lumbar inclusive. The white rami communicantes conduct them from the 
roots to the ganglia of the sympathetic chain situated along the front of the 
vertebral column, from which point they take varied courses according to their 
destination. 

On leaving the cord (Starling), the vascular nerve fibers carrying vasoconstrictor 
impulses come to an end in a collection of ganglion cells that either belong to the main 
chain of the sympathetic or are situated more peripherally belonging to a group of collateral 
or peripheral ganglia. The fibers leaving the central nervous system are small medullated 
nerves that end in the ganglion by arborescing around ganglion cells from which a fresh 
relay of fibers carries the impulses to the muscle fibers of the blood vessels. 

The splanchnic nerve is regarded as the most important vasomotor nerve of the body. 
It receives most of the fibers from the lower seven dorsal and upper two or three lumbar 
roots, the latter fibers often taking a separate course as the lesser splanchnics. Experi¬ 
mental section of the splanchnic in herbivorous animals, in which the alimentary canal is 
very much developed, causes a marked fall in general blood pressure. 



FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 


37 


Vasodilator Nerves.—Whilst at first it was believed that dilatation of 
arteries is produced only by inhibition of the normal constrictor impulses, 
another nerve supply antagonistic in function to the vasoconstrictors has been 
detected in many parts of the body. 

Genuine inhibitory nerves to the arterioles are assumed to exist, through 
which vascular dilatation is produced. This is to be expected and con¬ 
forms to the rule; for, smooth muscle not subject to voluntary control is 
usually supplied with two kinds of nerves, excitatory and inhibitory. 

Stimulation of the peripheral end of the chorda tympani nerve to the submaxillary 
gland, causes such marked vascular dilatation, that six to eight times the previous amount 
of blood is made to circulate. Amongst other vasodilator nerves we may mention, the 
lingual nerve to the blood vessels of the tongue, the small petrosal to the parotid gland, and 
the nervi erigentcs to those of the penis. 

It is a mooted question as to whether vasodilator fibers are present in 
the nerves of the limbs. In experimental stimulation the vasoconstriction 
produced more than counterbalances any results obtainable through the 
simultaneous excitation of possible dilator fibers. The dilators apparently 
do not conduct any tonic influences to the blood vessels, so that the only 
effect of section of a mixed nerve is that due to the removal of the tonic 
constrictor impulses, and the vessels in the area of nerve distribution become 
dilated. 

Physiological researches have shown that vasodilator fibers course in the sciatic nerve. 
The dilator fibers, however, cannot be traced back through the sympathetic system. The 
observation of Strieker and Morat that dilatation of the vessels of the hind limb can be 
produced by stimulating the posterior roots of the nerves going to the limb, was confirmed 
by Bayliss. According to Starling “Stimulation of the posterior roots, either before or 
after they have passed through the ganglia, causes dilatation of the vessels in the area of 
the supply of the roots, whatever be the nature of the stimulus employed, whether electrical, 
chemical, or mechanical. This effect is not destroyed by previous section of the posterior 
roots on the proximal side of the ganglia, showing that the fibers by means of which the 
dilatation is produced have the same origin and course as the ordinary sensory nerves to the 
limbs. Since the vasodilator impulses pass along these nerves in a direction opposite to 
that taken by the normal sensory impulses, Bayliss has designated them as antidromic 
impulses. So far this phenomenon of a nerve fiber functioning (not merely conducting) 
in both directions, is almost without analogy in our knowledge of the other nerve functions 
of the body. There is no doubt, however, that similar antidromic impulses are involved in 
the production of the so-called trophic changes, such as localized erythema or the formation 
of vesicles (as in herpes zoster ), which may occur in the course of distribution of a sensory 
nerve, and is always found to be associated with changes, inflammatory or otherwise, in the 
corresponding root ganglia. Moreover evidence has been brought forward that these 
fibres may take part in ordinary vascular reflexes of the body, that in fact they are normally 
traversed by impulses in either direction.” 

In the antidromic vasodilatation, and in the reddening and inflammatory changes 
consequent upon local excitation, Meyer and Bruce believe that impulses course by way of 
axon reflexes, these being the remains of local reflexes of a primitive peripheral subcutaneous 
nervous system. All the signs of a local inflammation can be produced by the application 
of croton oil to the skin or conjunctiva. Nor will destruction of the central nervous system 
or section of the sensory nerve roots (posterior spinal root or trigeminus) on the central 
side of the ganglion alter the reactions. If, however, a division peripherally of the gan¬ 
glion be produced and time be allowed for complete degeneration of the nerve fibers to their 
peripheral terminations, the application Jof croton or mustard oil, even to the delicate 
conjunctiva, is without effect. Similar Vesults follow when the peripheral terminations 
of the nerves are paralysed by the subcutaneous injection of local anesthetics. Starling says 
that we must assume that the axons of the peripheral sensory nerves branch, some branches 
going to the surface, others to the muscle-cells of the cutaneous arterioles. 

While Bayliss expounded the theory of antidromic conductivity in the sensory nerve 
fibers, some of the more recent Continental observers reject this view. According to 
Bayliss both centripetal sensory impulses course in the sensory fibers to the posterior nerve 
roots, as well as coincidental centrifugal vasodilator impulses. Continental observers 
regard this as artificial explanation, all the more so, since existing well-known nerves have 


38 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


been demonstrated to conduct both centripetal sensory and centripetal vegetative functions. 
As an example may be mentioned the vagus nerve and the chorda tympani, composed of 
sensory and parasympathetic nerves. By analogy it could be assumed, therefore, that 
other nerves in communication with the spinal cord could be similarly constituted. 

Recent Views.—Recently the Continental school of investigators have 
made contributions somewhat at variance with the findings of the English 
physiologists who were largely responsible for the foregoing facts. 

Embryologically the heart forms a part of the total vascular system from 
whence it would appear probable that both heart and peripheral vessels 
receive parasympathetic and sympathetic innervation. It is believed that 
heat regulation depends for the most part upon changes in the transverse 
section of the blood vessels; that cooling produces an irritation of the para¬ 
sympathetic and heating a similar response in the sympathetic paths. Up 
to the present time, however, double vascular innervation has been dis¬ 
covered for but a small portion of the vascular tree. 

It is known that the parasympathetic dilator fibers of the chorda tympani pass through 
the vessels of the salivary glands; and that vasoconstrictor fibers from the cervical sym- 
pathetics pass to the same vessels. The double innervation of the vessels of the penis is 
even more significant. Here vasodilator impulses pass through the N. erigens from the 
sacral cord (containing parasympathetic fibers of erection), while vasoconstrictor sympa¬ 
thetic fibers (from the lumbar cord) occasion relaxation. 

In spite of the warrantable conclusion, concerning a double antagonistic 
peripheral innervation of the vessels acceptable through analogy and physio¬ 
logical considerations, no definite anatomical corroborative evidence is yet 
at hand to prove that the vascular nerves of the skin of the trunk and extrem¬ 
ities contain parasympathetic fibers. Langley is largely responsible for the 
view that the points of origin of the thoracic and lumbar vegetative fibers 
contain only sympathetic fibers. Dresel, Brugsch, Kraus and others express 
the conviction, however, that this is no longer in accord with modern evidence. 
Basing their deductions upon the well-known double vegetative inner¬ 
vation of the striated muscles; upon the course of the nerve fibers of the sweat 
glands; and finally, upon the essential requisite for a parasympathetic vaso¬ 
dilator fiber supply to the vessels of the trunk and extremities:—they believe 
that such combinations of sympathetic and parasympathetic cells of origin must 
reside in the thoracic and lumbar cord. For such a coincidence is accepted for 
the dorsal vagus nuclei. Of late, Muller extends the hypothesis of Bayliss, 
regarding the existence of vasodilator fibers in the posterior roots, into the 
theory that such paths are constituted of parasympathetic nerves. In 
short, enough data are at hand to allow of the assumption that preganglionic 
parasympathetic ganglion cells may exist in the thoracic and lumbar cord, 
from which the striated musculature, sweat glands, and vessels receive addi¬ 
tional innervation. Dresel agrees with Muller that we must reject the old 
view that a dominant vasomotor center exists in the medulla oblongata. 

As for the vasomotor reflexes, an arc is thought to exist, one of whose 
limbs is constituted by centripetal sensory fibers, with a relay station in the 
cord, through which the impulses then travel through the centrifugal vegeta¬ 
tive paths. Such reflexes can be demonstrated after section of the cord, 
even in the anesthetic territory. 

Nerve Influences in Capillary Motility. —Whilst admitting that chemical 
or humoral factors are capable of influencing the caliber of the capillaries, 
Krogh has recently rejected his original view that the nervous system does 
not play an important role in capillary activity. In his latest investigation 
on the submucous capillaries in the tongue of the frog this author has shown 


FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 


39 


that the capillary dilatation following local trauma is brought about by nerve 
action. A reflex is established in the sensory nerves; and its course would 
follow an antidromic direction (axon reflex) directly opposed to that of the 
sensory impulses (Fig. 27). 



Fig. 27. —Scheme of vasomotor innervation in the responses of capillaries to local 
mechanical irritants. A, arterioles; S, nerve sectioned. I, A stimulus at X travels over 
sensory filaments in the direction of the arrow and in antidromic direction back so as to 
innervate the capillaries; II, shows that the capillary response is maintained even after 
nerve section; III, shows that the capillary reaction is absent when secondary nerve degen¬ 
eration has taken place. ( Krogh ) 


These conclusions are based upon the following findings: A puncture trauma brings 
about capillary dilatation (except when the wall of an arteriole is injured, when contrac¬ 
tion is induced). Immediately after section of the motor and sensory nerve of the region 
under experimentation, no change in the capillary response after puncture follows. Such 
a result would seem to be independent of the nervous system. But, if the experiment is 
repeated after degeneration of the nerve has taken place, the dilating response of the capil¬ 
laries is absent. Similarly, local cocainization suppresses the reaction. 

Experimental work has shown that section of the spinal cord in animals 
is followed by an immediate dilatation of all the vessels below the level 
of the section in the territory supplied by nerves arising below the level of 
section. Afterwards, however, the vessels contract again, an evidence of 
functional control in the spinal cord. These facts would tend to corroborate 
the assumption that the higher centers only motivate the vessel activities. 
Moreover, destruction even of these portions of the spinal cord is not fol¬ 
lowed by complete loss of all vasomotor innervation. Although there is 
temporary vascular paralysis, this gives way to normal vascular constriction 
after a time. A normal tone of vessels may persist in animals even after 
the central nervous system has been excluded as a factor in the regulating 
mechanism. From this it has been deduced that a peripheral nervous appara¬ 
tus or local vascular center must exist. This is represented by the ganglion 
cells and plexuses that surround the vessels. 

Although total loss of the cerebrospinal system is followed by a reduction 
in the total responsive capacity of the vessels (in animals), nevertheless 
Lewaschew 1 was able to show that vessels whose vasomotors were paralyzed 
still gave the well known reaction of contraction and dilatation to changes in 
temperature. The usual vessel activities or responses to direct mechanical, 
thermic, chemical and electrical irritation of the periphery are said by 
Landois to take the circuit of the peripheral vessel ganglia. In such func¬ 
tions the paths would be axon reflexes (Langley 2 ), that is, within sympathetic 
neurons. True reflexes, however are not confined within the sympathetic 
system, but usually go through the cerebrospinal paths. 

lewaschew, Virchow’s Arch. f. path. Anat., 92, p. 152. 

2 Langley, Ergebn. d. Physiol., II, 2, p. 818. 



40 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Even the veins may contract upon external irritation. Constrict or 
phenomena are attributed to the venules in some forms of acroasphyxia. 1 
Although there is no accord amongst authors regarding the certainty of the 
presence of vessel centers, it may be accepted as proven that a certain auto¬ 
matism of peripheral action is a characteristic of the sympathetic system. 

The Vasodilator Function. —The action of the vasodilators is demonstra¬ 
ble when, after section of a nerve, irritation of its peripheral end is followed by 
dilatation of the innervated vessel, whilst the mere interruption of continuity 
produces no constriction of the lumen. The vasodilators do not appear to 
have influence upon the nor mal tone. Up to the present time no center has 
been found for these, although one is said to exist in the medulla oblongata. 
The course of the vasodilator nerves is still uncertain. In some organs they 
course as special nerves; in other parts of the body they are mixed with the 
vasoconstrictors. According to Strieker and Gartner 2 the plexus sacralis 
contains vasodilator nerves for the lower extremities. 

In the case of the vasodilators, also, subordinate centers are assumed to 
reside in the spinal column. Just how the vasodilators* work, has not been 
discovered. Some believe fthat their action is direct upon certain longitudi¬ 
nal muscles in the vessels. The view that they act in an inhibiting fashion 
on the peripheral ganglia is more acceptable. Others (Lewandowsky) assume 
that the vasodilators act directly upon the circular muscles of the vessels 
without intervention of peripheral ganglia, making these yield their tone. 

Excitation of the vasodilator center may be brought about directly or 
reflexly. When venous blood or a poison, such as chloral hydrate is given in 
small doses, a direct effect is produced; or, reflexly, as in erection, through 
sensory stimuli. Even the body temperature may be influenced through irri¬ 
tation of these centers. 

Antagonistic Innervation of the Vessels. —According to Muller 3 it is 
believed that the regulation of the size of the vessel lumina is also under the 
control of two separate systems of antagonistic action, namely, from the 
gangliated cord of the sympathetic and from the parasympathetic autonomic 
system. Such is the case in the other visceromotor functions. 

The relations that obtain in innervation of the vessels of the trunk and 
extremities are somewhat difficult of interpretation. The rami communi- 
cantes from the anterior roots appear to contain only vasoconstrictor fibers. 
Clinical facts point to the possibility of the transmission of vasodilator influ¬ 
ences from the posterior horns through the posterior roots, whence they attain 
the periphery through the spinal ganglia. Strong irritation of sensory nerves 
leads to active hyperemia in the irritated territory. This is a reflex pheno¬ 
menon, for after section of the nerve with interruption of the reflex arc, the 
hyperemia is absent. 

Whether the vasodilators are also in communication with ganglia of the 
gangliated cord, is doubtful. Bayliss was able to produce vascular dilatation 
in the lower extremity after irritation of the posterior roots, even when the 
abdominal sympathetic was removed. 

Not only is it accepted to-day that there are antagonistic double innervating 
paths for contrictor and dilator impulses, but it would seem that the conductivity 
of the dilator fibers persists longer than that of the constrictor paths (Muller). 

Still it is not necessary to assume that two separate centers must 
be present in the brain for vasodilatation and vasoconstriction. Indeed, 

1 Briscoe, see Chap. VII. 

2 Strieker & Gartner, Wien. klin. Wchnschr., 1889, p. 980. 

3 Muller, Das Vegetative Nervensystem, 1920. 


FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 


41 


the sudden blush of the face could hypothetically be brought about through 
paralysis of the vasoconstrictor center. It is more plausible that from a 
single vasomotor center influences emanate that simultaneously are of an 
inhibiting nature, and others of an exciting or vasoconstricting quality. 

Physiology of the Large Vasomotor Centers.—Physiologists believe that 
the vasomotor centers are ordinarily in a state of mid-tonic excitation. From 
them impulses are constantly flowing that induce a middle grade of contrac¬ 
tion of the vessel musculature, thereby producing the normal vascular tone. 
Fluctuations in the state of activity of the centers run parallel with the 
respiratory movements. According to Simon the function of internal secre¬ 
tions expresses itself in the production of hyper- or hypotension. These 
effects are in a state of equilibrium under physiological conditions. 

The vasomotor centers may be directly or reflexly stimulated. Direct 
excitation results from the action of the gas content of the blood circulating 
in the medulla oblongata. A marked venous admixture causes correspond¬ 
ingly strong stimulation of the center leading to contraction of the arteries. 

Irritation of certain centripetal nerves can produce contrary reflex effects 
either exciting or depressing the centers (pressor and depressor nerve fibers). 
Some authors believe such fibers are present in all sensory nerves. According 
to Loven irritation of sensory nerves causes firstly pressor effects; but con¬ 
tinued and intensive stimuli lead to depressor effects and vascular dilatation. 
Weak electrical or tactile stimulation of the skin, or thermic influences call 
forth depressor effects. 

According to certain authors, pressor effects can be obtained in a reflex 
way through the action of weak electrical irritation or through the applica¬ 
tion of cold or warmth to the skin. Hallion and Comte 1 produced vasocon¬ 
striction in a reflex way through various sensory irritants. Experimental 
investigation has shown that most of the irritants produced vascular constric¬ 
tion. Some authors have tried to show that sensory regulating fibers are 
present in the vessels themselves. 

The nerve control of the vessels differs somewhat from that of other organs 
whose activities are influenced by the vegetative nervous system. In the 
organs, peripherally situated ganglionic cells (such as the Auerbach plexus) 
take up impulses that modify the activity of the organs themselves. They 
are regarded as peripheral reflex or automatic centers, and have been com¬ 
pared to differentiated anterior horn cells. As such, motivating and inhibit¬ 
ing extracentrally situated sympathetic and parasympathetic nerves con¬ 
stitute the path for nerve control. But these reflex and automatic centers 
of ganglionic nature appear to be absent wherever the function is an uncom¬ 
plicated one as in the case of the vessels. 

Edinger believes that sensory impressions are produced on sympathetic 
cells lying directly in the vessels; and from these cells reflex contractions may 
take place in the arterial wall through other fibers. 

It is well known that section of the cervical region of the sympathetic 
brings about reddening and warmth of the ear of the corresponding side in 
experimental animals. The vessels dilate and the blood stream in the 
affected part is retarded. The blood pressure is increased, the arteries pulsating 
actively, the pulse even being noticeable in the veins. Irritation of a periph¬ 
eral vasomotor nerve itself brings about pallor of the corresponding part, 
coolness, reduction of temperature, and constriction of the vessel. In the 
case of smaller arteries such constriction can be so marked as to completely 

1 Hallion & Comte, Arch. f. Physiol., 1894, p. 381; 1895, p. 90. 


42 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


occlude the lumen. Continued excitation, however, finally brings about 
exhaustion of the nerve with the manifestations of paralysis.* These 
observations are of exceedingly great clinical interest in that they give us a 
clue as to the pathogenesis of many of the vasomotor affections, such as erythro- 
melalgia, Raynaud’s disease and the cases of vasomtor instability. 

It is an important observation that the effect of irritation or paralysis of vasomotor 
nerves varies considerably in intensity in different vascular territories. For instance, the 
vessels of the ears, nose, fingers and toes are most easily influenced, other regions being less 
intensively acted upon. These varying effects may depend to a certain extent upon the 
architecture of the arteries. 

The Vasomotor Tonus. —It is not necessary to assume that there are 
cirsumscribed areas controlling vegetative innervation of vasomotor func¬ 
tion. The dominating vasomotor center in the brain appears to functionate 
in conserving and regulating the general vascular tonus. Various emotional 
states are believed to cause qualitative alterations in the cranial vasomotor 
centers, from whence fluctuations in tonus are produced through activation 
of vasomotor centers in the cord. We do not know whether the tonic 
influences from the mid-brain are necessarily intimately connected with 
nerve fibers, or whether they are conducted through the gray substance, or 
through the substantia gelatinosa. For, as in electricity, special conducting 
paths are not essential. Muller designates the status of the general' nerve 
excitability as a biotonus 'which may suffer alterations under various con¬ 
ditions. Particularly in the spinal cord are such changes possible, as mani¬ 
fested by increased intensity of reflexes during emotional states. This 
tonus may also be susceptible to sensory impulses. And, therefore, the 
theory has been proposed that pain impulses, or other tactile sensory impulses, 
may cause a generalized change in excitability of the gray substance of the spinal 
cord. Such modification in the tonus of the spinal cord would in turn react 
on the function of the spinal vegetative centers, such as the vasomotor cell 
group. This theory is supported by the belief that it is quite impossible 
for all sensory paths to be in immediate connection with all vegetative centers 
in the spinal cord, medulla oblongata and mid-brain. Clinically, note¬ 
worthy is the great vasolability manifested in the lower extremities of 
thrombo-angiitis obliterans and to a less degree in the extremities affected by 
atherosclerotic and other arterial disease. In the former malady it not infre¬ 
quently follows persistent pain. It is more than likely, that just such a tonus 
alteration in the spinal cord, in consonance with the above hypothesis, may 
obtain in thrombo-angiitis obliterans, and account for the vasomotor lability 
of many of the cases. 

The tonus that dominates the spinal vasomotor centers appears to be reestablished in 
the distal portions of the spinal cord shortly after experimental section of the spinal cord. 
It fluctuates according to the sensory impressions that arise in the detached portion of the 
spinal cord. After total section, irritation of the sciatic nerve produces increase in blood 
pressure. When the feet in a paraplegic are exposed to cold impulses, the subsequent 
vasoconstricting effect is limited to the lower part of the body. This observation seems 
to speak for the view that the dominating tonus in the spinal vasomotor centers is conducted 
not through long isolated paths, but rather controls the whole of the gray substance and 
varies or is changed through numerous sensory influences. Of these latter, pain and tem¬ 
perature are the most important. Such impulses do not necessarily come to our conscious¬ 
ness, nor reach the cranial vasomotor centers, as is exemplified by the paraplegic. It 
would appear that the alteration in tonus occupies the total transverse area of the cord, 
since on the action of cold, not only vasoconstriction but simultaneous pilo-erections, con¬ 
traction of the scrotum and the skin of the penis, as well as contractions of the striated 

1 Compare with explanations of erythromelia in Chap. XLI. 


FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 43 

muscles are observed. It is also noteworthy that heat elicits dilatation of the vessels, 
sweat and relaxation of the scrotum. 

Histologically the cells resemble the ganglion cells in the sinus nodes and in the auricular 
septum of the heart. The small ganglion cell group and the single cells that are sometimes 
found in small nerve bundles are found in loose connective tissue of the adventitia. Although 
such cells have been found in the vessels leading to the viscera cells and in the aorta, they 
have not been demonstrated thus far in the vessels of the extremities. 

It is not unlikely that in the neighborhood of the vessels, or in the vessel 
walls, peripheral vasomotor centers capable of an automatic tonic function 
exist. These have been called vasomotor centers of the third class in contra¬ 
distinction to the first (cerebral) and second (spinal) category. It is be¬ 
lieved that the vessel activities resulting from direct irritation take place 
through the intervention of these centers. Indeed, by means of special 
tinctorial methods, nerve elements have been demonstrated in the vessel 
walls. 

According to Glaser 1 it is possible to demonstrate a network of fibers in the adventitia 
of the veins if we employ vital stains and young subjects. A further network of nerves is 
seen between adventitia and media; also between the muscle bundles of the media, a branch¬ 
ing network of finest fibrils with knobbed nerve filaments has been found. Some of these 
travel the whole media and penetrate into the intima. These appearances have been 
demonstrated for all of the larger arteries and veins. Even the capillaries are enmeshed 
with nerve filaments that show numerous anastomoses. 

In the deeper layers of the vessels ganglionic cells have not been found. 
Inasmuch as ganglionic cells have not as yet been demonstrated in the 
peripheral arteries, we cannot exclude the possibility of direct muscular ves¬ 
sel reactions to mechanical or thermic stimuli. 

As for the distal constrictors and vasodilators very little is known. Indeed, the old 
concept that the vasoconstrictors lead to the annular musculature and the vasodilators to 
the longitudinal muscle fibers has not been conclusively proven, all the more so, since the 
smallest vessels contain no distinct longitudinal muscle bundles. 

Recent Views on Physiology. 2 —The peripheral parasympathetic and 
sympathetic fibers have an antagonistic influence upon the single vegetative 
organs. Dresel believes that alterations in the functional condition of the 
cells (muscle or glandular cells) may be brought about through nerve impulses 
coursing through this system; and that the modus operandi is one in which the 
surface tension or potential undergoes a change. Such deviations may be 
produced in the electrolytic equilibrium of calcium and potassium, with the 
balance in favor of one or the other Ion. This with other biochemical altera¬ 
tions would effect functional derangements in the cells (such as muscle and 
gland cells). 

A coordination of the antagonistic effects of the parasympathetic and 
sympathetic nerve impulses is realized through the central vegetative nerve 
stations. The view until recently widely accepted, to wit, that irritation of 
one system induces a diminution of tonus in the other system (Eppinger 
and Hess), seems to be controverted by recent investigations. Thus it has 
been shown (Dresel) that every parasympathetic excitation is followed by 
one of the sympathetic and conversely. The mechanism responsible there¬ 
for is one that tends to conserve the dominant equilibrium. This is accom¬ 
plished through a regulating mechanism in the subthalamic center, which 
responds to every change of temperature, of blood pressure, or of blood 
sugar content, by influencing the subordinate parasympathetic and sympa- 

1 Miiller, loc. cit. 

2 Personal communication from Kurt Dresel of Berlin. 


44 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


thetic cell origins. For example, if the blood pressure increases by virtue 
of irritation of the sympathetic (adrenalin) a parallel stimulation of the para¬ 
sympathetic paths follows through this regulating mechanism, with the pur¬ 
pose of limiting an inordinate increase of pressure and of restricting it to a 
certain threshold. These phenomena may be compared with the well-known 
manifestation of successive induction (Sherrington) occurring in the animal 
nervous system. According to this view, coincidently with every reflex, 
agonistic as well as antagonistic impulses are evoked to check excessive 
motion. 

The above-described regulation may be motivated through the direct 
action of chemical and physical blood changes upon the subthalamic centers 
(of temperature, sugar content, Ion content, blood pressure, etc.). The sub¬ 
thalamic center takes a subordinate position to that in the corpus striatum, 
for the latter is in control of the vegetative function. Indeed, it is believed 
that the impulses emanating therefrom determine the threshold. This 
threshold (for temperature, blood sugar, Ion concentration and blood sugar) 
may be attuned to different levels, through alterations in excitability and 
state of excitation of the striate body. 

Dresel compares the activity of the vegetative centers with a thermostat in which the 
above functions may be symbolized. The mechanism for regulating heat can be set for 
varying degrees such as 42 0 C., 37 0 C., or 26° C., through the action of the center in the 
corpus striatum. Just as the regulatory mechanism of a thermostat reacts to changes of 
externaljjtemperature, so also do the subthalamic centers, whose function it is to conserve an 
equal temperature; and this is effected in that the subordinate centers (points of origin of 
the parasympathetic and sympathetic in the mid-brain, medulla and cord) are made to 
respond accordingly. Similarly for all other vegetative functions there is a very accurately 
and delicately attuned mechanism for the conservation of proper equilibria. It is then 
easily understood how very slight alterations may bring about very severe symptoms. 

The Vascular Nerve Centers .—It has already been previously mentioned 
that the cellular points of origin for the peripheral vegetative vascular nerves 
are to be found in the medulla and in the spinal cord, where they receive 
their impulses from the superior vascular centers in the subthalamic regions 
and corpus striatum. Karplus and Kreidl had already demonstrated the 
existence of nerve communications between the subthalamic region and cord 
(since irritation of the mid-brain failed to produce typical effects on the vessels 
after section of the cervical cord). Dresel obtained anatomical proof in 
the finding of retrograde degeneration in the cells of the subthalamic region 
after section through various levels of the spinal cord. Furthermore, this 
author showed that certain ganglionic cells in the subthalamus undergo 
variation in excitory state, through fluctuations of blood pressure. 

It is well known that clamping or ligation of the carotid leads to increased blood pressure 
in the arteries (with the brain excepted). Such hypertonia results through regulatory 
impulses emanating upon the mid-brain. That such must be the case was proven by the 
absence of such an eventuality after section through the corpora quadrigemina. So it has 
been assumed that the regulatory impulses leading to increased blood pressure are evoked 
through the diminished blood supply in the brain, and have their source in the mid-brain. 

Analogous phenomena are to be found in the so-called “vagus pulse.” This follows 
injection of adrenalin, and has been said to be due to direct action of adrenalin or increased 
blood pressure upon the vagus center. Perhaps, however, this vagus effect is nothing but a 
manifestation of regulatory impulses from the mid-brain, in response to the increased blood 
pressure. This conclusion is warranted on the basis of the observation, that the vagus pulse 
can be prevented by preliminary separation of the medulla and corpora quadrigemina 
through section (whence adrenalin injection will be ineffective in spite of the continuity of 
the peripheral nervous system). Although Karplus and Kreidl had already noted the 
vasoconstrictor effect that follows direct electrical irritation of the hypothalamus, no 
functional conclusions were drawn by these authors concerning blood pressure phenomena 
in general. 


FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 


45 


The corpus striatum is said to have a distinct influence upon the vascular 
nerves and upon blood pressure (Dresel). 

If a point in the nucleus lentiformis (globus pallidus) is accurately stimulated with a 
double electrode, the introduction of faradic current brings about considerable fall in blood 
pressure, which continues for a time after cessation of the electric irritation and then 
gradually disappears. 

Here we see then that there is a distinct relationship between blood pres¬ 
sure level and the excitatory condition of the corpus striatum (just as is the 
case with the thresholds of other blood components). \- 

The psychic and sensory influences upon the whole vegetative nervous 
centers probably take place by way of the center in subthalamic and striated 
centers. Here, then, there is disparity between animal and vegetative 
nerve functions. In the former , actual areas of projection in the cortex of the 
brain exist , while the absence of such for the vegetative system would seem to have 
been confirmed by researches. For, dogs without cerebral cortex may be 
wholly devoid of any vasomotor disturbance. 

In the vegetative system, changes of vascular girth run parallel with changes in total 
metabolism. With such vascular alterations there is usually a generalized reversal, 
inversion or modification in the vegetative system. 

Then again the question has been ventilated as to whether delimited vascular territories 
are represented in the circumscribed vegetative centers. Indeed, experimental and clinical 
experiences would seem to point to the possibility that certain ganglionic cells do control 
the regulation of certain vascular territories. It has been even suggested that excitatory 
changes in the centers of the striatum and hypothalamus may be induced so as to bring 
about limited vascular alteration in an extremity. Emotional impulses are said to evoke 
such phenomena. Since cortical centers are absent, the separation of vascular territories 
in central stations must needs take place at a higher level than at the points of origin of the 
peripheral vasomotor nerves (medulla and cord). 

Viscero-vasomotor Reflexes or Vaso-vasomotor Reflexes. —Clinical observa¬ 
tions have suggested that not only do viscero-sensory reflexes exist as exem¬ 
plified by the Head zones, and visceromotor reflexes as in the so-called 
“ defense musculaire,” but that there may be viscero-vasomotor responses 
or even vasomotor responses secondary to irritations of vascular origin. 
Zak 1 describes hyperemic or erythematous zones below the fossa jugularis, 
and just under the mesial half of the clavicle in cases of aortic disease. These 
areas are roughly of semilunar shape, and the skin in this region responds 
with abnormal activity to mechanical irritation. In some cases the vaso¬ 
motor centers are hyperirritable through impulses sent from the diseased 
aorta; in others, the centers themselves are primarily in a state of increased 
irritability. 

Other visceral affections such as pulmonary diseases may give similar vasomotor zones. 
Zak states that in about one-third of the cases of aortic disease distinctly demonstrable 
semi-lunar erythematous manifestations are present; and that these are evidences of local 
vasomotor hyperexcitability with corresponding segmental alterations in the spinal centers. 
There is a certain degree of parallelism between the vasomotor and sensory hyperexcitability. 

Miiller 2 describes a clinical method based in all probability upon reflexes through the 
spinal segment corresponding to that irritated. A ring is pressed against the skin, and 
the included cutaneous area rubbed energetically with the end of a match-stick, so as to 
produce a somewhat painful sensation for a period of io seconds. Thirty to 60 seconds 
later and after the cessation of the painful irritation there will arise in addition to the 
hyperemia within the boundary of the ring, a second hyperemic zone extending for a 
considerable distance beyond, the direction of this rubor being in accordance with the 
cutaneous segments, that is, more or less vertically over the arm, horizontally over the 
trunk. 

1 Zak, Wien. klin. Wchnschr., 25, 1920, also Wien. Arch. f. klin. Med., IV, p. 209,1922. 

2 Muller, Ztschr. f. Nervenh., 47, 48, 1913. 


46 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Goldscheider, 1 in some clinical experiments applied a clamp to pinch the skin for i or 
1 3 ^ minutes. Besides the manifestation of pain and a cutaneous areola of rubor, an addi¬ 
tional girdle-like hyperalgesic zone appeared over the trunk, or a longitudinal vertical 
streak over the extremities. Similarly a hyperemic zone developed presumably through 
reflexes passing by way of the spinal segments. > ...... 

Therefore, just as a cutaneous zone of hyperalgesia corresponds to a state of irritability 
of the sensory fibers and ganglionic cells of the corresponding segments, so also, it is now 
believed that an increased excitability of the vasodilator centers may take place. There¬ 
fore, in addition to so-called viscero-sensory reflexes and visceromotor reflexes, a viscero- 
vasomotor reflex may occur ( Mackenzie ). 

These observations give further foundation in analogy to the warrantable 
assumption that through disease of the arteries, as in thrombo-angiitis 
obliterans, and partly by reason of the pain impulses often or continuously 
traveling in such cases, vasomotor reflexes establish themselves, and are 
responsible for the increased vasolability (vasomotor neurosis) observed in 
such cases; and perhaps also for the rubor under certain conditions. 2 

Pain and the Sympathetic. —The exact role of the sympathetic system in 
the production of pain is not known. There seems to be no doubt but that 
centripetal impulses occur in the sympathetic system, and further, that 
stimulation of these fibers may occasion pain. The origin of a pain of sympa¬ 
thetic causation probably depends upon the quality of the irritant. Num¬ 
erous theories have been advanced to explain vascular pain. We know that 
pressure upon arteries produces painful impulses. Stimulation of the centri¬ 
petal nerve fibers of the blood vessels, even though unproductive of pain 
sensation under ordinary circumstances, may produce such in exceptional 
conditions. Dogiel asserts that the perivascular tissue usually contains 
medullated nerve fibers, and Vater-Pacini bodies occur in the adventitia. 
Cassirer believes that direct irritation of the vessel wall through its sensory ele¬ 
ments accounts for the pain in erythromelalgia; for, the vasomotor and sensory 
irritative symptoms roughly correspond in their distribution. In the aero - 
paraesthesiae irritative conditions of the vasosensory fibers may also be 
responsible for the symptoms. 

Summary of the Vasomotor Mechanism.—A reference to Fig. 27 will tend to clarify the 
concept of the mechanism of vasomotility. Through the four neurones, (a) cerebro- 
bulbar, ( b ) bulbospinal, (c) spinosympathetic, and ( d) sympatheticomuscular, the brain 
and the three relays are brought into communication with each other and with the peri¬ 
phery. Since vasodilator fibers have only been found in certain special regions, they are 
not represented in this schematic drawing. Generally speaking, we regard loss of vascular 
tone as due to vasoconstrictor paralysis, and vasoconstriction as the result of vasomotor 
stimulation. 

It is comprehensible then, that a lesion of the ventral horn is followed by vasomotor 
paralysis if a discontinuity between the third set of neurones (cinFig. 27 a) and the central 
cell group is effected. So also, breaks in the connections of the bulbar and spinal centers 
(b) through lesions of the lateral columns may have the same result. 

According to Bing, 3 spinal vasomotor paralysis, whether produced by destruction of the 
vasomotor centres in the ventral horn, or by interruption of the vasomotor fibers in the 
lateral columns, seldom reveals itself, and then only in its earliest stages by redness and 
heat of the skin. The skin in the territory innervated by the affected regions of the cord, 
becomes cold and cyanotic, a condition that may ensue forthwith after the occurrence of 
the lesion, or may replace a transitory hyperemia. 

A glance at the vasomotor paths will demonstrate at once that central lesions inter¬ 
rupting paths in the spinal cord would have an action over extensive circulatory territory. 
The local manifestations of vasomotor derangement seen in the diseases described here, are 
limited to such an extent as to warrant the supposition that either more peripheral disorders 
of innervation are responsible, or isolated ganglion or horn cells only partake in the neurotic 

1 Goldscheider, Ztschr. f. klin. Med., 85, 1918. 

2 See Chapters XLVI and L (Erythromelia and Pain in Thrombo-angiitis). 

3 Bing, R., Regional Diagnosis in Affections of the Brain and Spinal Cord, Transl. 
Rebman, New York, 1913. 


FUNCTIONS OF THE VASOMOTOR NERVOUS MECHANISM 


47 


disturbances. A more detailed discussion will be found under the chapter on the “Vaso¬ 
motor and Trophic Neuroses.” 

In forming a correct concept of the vegetative functions we should not 
confine their paths to the gangliated cord, but include as important elements 
the higher centers in the spinal cord and brain. Although exact localization 
of lesions that could evoke certain vasomotor neuroses is as yet not feasible, 
enough data are at hand to make us suspect that the intermedio-lateral region 



of the posterior gray substance may be the seat of some of the causal lesions 
in certain of the vasomotor and trophic disorders. But derangements in 
the reflex arcs, too, can be regarded as etiologic factors. . 

Cassirer expresses the view that a disturbance in the reflex mechanism 
between sensory and vasomotor systems could account for many of the cases 
of vasomotor and trophic neuroses and their trophic lesions of the skin. 

Various hypotheses have been offered as to the course of the. reflex, arc, 
alterations in which may lead to vasomotor and trophic manifestations. 
Vasosensory fibers may exist and make a portion of the afferent elements of 
the sympathetic. Excitation of these is believed to account for the extent 
and quality of the peculiar pains of which cases of. vasomotor and trophic 
neurosis complain. So, too, in thrombo-angiitis obliterans it is not unlikely 
that some of the varied forms of pain, particularly those associated with a 
state of marked vasomotor instability may owe their origin to the excitation 
of vasosensory nerves (Chap. L). 








48 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In further support of the reflex theory of vasomotor innervation, is the 
circumstance that irritation of sensory nerves has a greater influence on 
vasomotor tone (especially vasodilatation) than mere section of the sympa¬ 
thetic. The reflexes need, however, not be confined to the sympathetic 
system, a territory within which such phenomena do not seem to take place, 
but may take place through the intervention of additional spinal sensory 
paths. 


CHAPTER VI 

PHYSIOLOGY OF THE PERIPHERAL CIRCULATION 

Elementary Principles. —It may not be amiss to summarize some of those 
fundamental facts concerning the general circulation that have a direct 
bearing on the blood flow in the extremities. 

Although the laws governing a constant flow of fluids through rigid 
tubes apply to those with elastic walls (as arteries and veins), a distinct differ¬ 
ence exists when fluid is forced into these intermittently and rhythmically. 
Fluid thus driven into rigid tubes is evacuated interruptedly; in elastic 
tubes, however, an intermittent pulsatile stream may be converted into a con¬ 
tinuous one. The distended elastic walls of the tube exerts such pressure 
on the contents when the inflow ceases, that the current becomes continuous 
even during the pause in the main propelling force. 

With the heart as the pump, the elastic arterial walls act in this way, 
and, during the diastole the current in the capillaries is continuous. The 
arterial elasticity, therefore, is of considerable moment in its influence on 
the cardiac work. In view of the participation of the arterial walls in the 
propulsive mechanism, the total cardiac work is under normal circumstances 
commensurately lessened. 

The circulation of the blood conforms, then, to these principles and is 
modified by the vasomotor innervating mechanism. 

Let us briefly discuss here some of the hydraulic principles that govern 
the blood flow, in so far as they may clarify our concepts of the criculatory 
affections of the extremities; the nerve control and its influences shall be given 
consideration elsewhere. 

The volumetric increase of the arterial tree is proportionate up to a cer¬ 
tain limit to the internal pressure, only to diminish over this point. Fur¬ 
thermore, the more peripheral the arteries the greater the dilatation with 
equal increase in blood pressure. As the arteries become less elastic with age 
and disease, the nearer does their function approach the qualities of the rigid 
tubes. 

The pressure in, and the volume of blood delivered by the arteries are 
dependent on a number of factors; namely, (i) the supply to the heart; (2) 
the frequency and force of the heart beat; (3) the resistance in the arteries; 
(4) the viscosity of the blood; (5) the quantity of blood; (6) the changes in 
the flow under special circumstances; and (7), the changes in cardiac work. 

1. It is clear that the quantity of blood delivered by the cardiac pump must be related 
to that quantity which is emptied into the heart through the large veins. Many experi¬ 
ments have demonstrated that with other conditions unaltered the volume of blood deliv¬ 
ered per minute increases in proportion to that supplied to the heart. 



PHYSIOLOGY OF THE PERIPHERAL CIRCULATION 


49 


2. If a sufficient quantity of blood enters the heart through the veins to fill it during 
diastole, the volume of blood delivered by the heart per minute is directly proportionate to 
the frequency of the heart beat. Tins is true up to a certain limit only; for as the diastole 
becomes shorter its duration may be insufficient to permit of adequate filling of the heart. 
And so from this point on the amount of blood that is ejected during the systole becomes 
smaller and smaller until finally the volume per minute is less than that which the heart 
would deliver during periods of diminished activity. Whilst these facts are based on phys¬ 
ical laws, under ordinary circumstances it is maintained that the volume of blood delivered 
per minute, as well as the pressure, does not vary with the frequency of the heart beat within 
certain limits, when ever the resistance to the vessels remains unchanged. 

3. Increased resistance offered by the arteries may cause a rise in blood pressure. 
Contraction of the vessels in a large territory (or ligation of a large vessel as the abdominal 
aorta) increases the pressure. With moderate increase of the resistance the heart may 
either deliver an equal amount of blood during a unit of time, or a greater amount. In the 
latter case, rise of pressure follows. Should a marked increase of resistance take place, 
the quantity of blood delivered becomes smaller and finally stasis of blood in the heart may 
result. Nature has. provided a reflex mechanism, which, under certain circumstances, 
brings about dilatation of the arteries with commensurate relief to the heart (through the 
depressor 1 nerve, irritation of whose central end brings about fall of blood pressure). 
The autonomic action of the capillaries 2 is now recognized as capable of playing a dis¬ 
tinctive role. Krogh showed that most of the blood capillaries in a muscle when at rest 
are to be found in a state of contraction, their lumina not being too small for the passage 
of red blood corpuscles. This functional exclusion of the capillaries goes hand in hand 
with a reduction in the activity of the muscle fibers and with the diminution in the need 
of oxygen, glucose, etc. As soon as the circulatory demand becomes more active by virtue 
of enhanced muscular function, the caliber of the capillaries becomes greater, they dilate, 
and the flow of blood in the muscles becomes accelerated. In reality the contracted capil¬ 
laries are never completely closed, but allow the blood plasma to circulate. 

Besides this functional response on the part of the capillaries, alternate dilatations and 
contractions in certain of their territories may occur spontaneously from time to time by 
reason of chemical influences. 

4. Changes in the viscosity of the blood are said to alter the resistance offered to the 
circulation independently of alterations in the vascular patency. It has been shown that 
the internal friction of the blood in certain animals is 3 34 times as great as that of distilled 
water. The non-defibrinated blood of animals and of the human is believed to possess an 
internal friction of 4 to 5 times that of distilled water. After blood letting this friction 
diminishes; after feeding animals it increases. The viscosity of the blood also has been 
reported as being increased by multiplication of the red blood cells, and reduced by admin¬ 
istration of salt solution. With diminished viscosity, the heart may, in a unit of time 
deliver larger quantities of blood than normal without appreciable increase in the blood 
pressure. Perhaps this phenomenon explains the apparent improvement in the general 
condition and in the circulation of some cases of thrombo-angiitis obliterans after the 
administration of large quantities of Ringer’s solution subcutaneously or through the 
duodenal tube (Chap. LXV). 

5. The total quantity of blood is of no mean importance in determining the volume of 
blood delivered into the vessels. Increase of blood pressure may be obtained by inhibition 
of fluid through the intestinal tract, under the skin, and by transfusion, with consequent 
delivery of larger quantities of blood into the vessels. 

6. Exercises and physical work increase the frequency of the heart beat with consequent 
increased demands upon the circulation in the arteries. Increased blood pressure may 
follow and the volume of blood delivered per minute may increase from 3 to 7 times the 
normal. Other external influences (such as obtain with baths), influence the circulation. 
The hydrostatic pressure bath is known to exert a distinct effect on the circulation. 

7. The response on the part of the heart muscle to changes in the circulation must also 
be taken into consideration in an estimation of the quantity of the blood delivered. And 
so it is not always the greatest arterial pressure that evokes a corresponding cardiac activ¬ 
ity, but moderate demands or moderate increases of pressure. 

Measure of Blood Flow in Extremities. —Perhaps we could obtain a better 
appraisal of the adequacy of circulation in the peripheral part of a limb by a 
knowledge of the so-called mass movement of blood. It is conceded that 
arterial pressure is not in itself an index of the measure of the flow. 

1 This nerve crosses into the cardiac plexus, arises in two routes, one from the vagus, 
the other from the inferior laryngeal. 

2 See Chap, on Physiology of the Capillaries. 

4 


50 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Stewart 1 has suggested an ingenious method of measuring the blood flow, 
which he regards as simple and accurate enough for clinical purposes. The 
method is based upon the fact that the amount of heat produced by a part, 
like the hand during rest, is negligible in comparison with the heat conveyed 
to it by the arterial blood. Determination of the amount of heat given off to 
a calorimeter in a given time in its relation to the temperature of the arterial 
and the venous blood, permits of calculation as to how much blood must 
have passed through the part. 

Perhaps the wider adoption of methods such as these will prove of some 
value in the circulatory affections of the extremities. 

Some of the results obtained by the calorimetric measurement of blood 
flow through the extremities may be thus summarized (Stewart). 

In arteriosclerosis the blood flow in the hands is smaller, and the contra¬ 
lateral vasomotor reflexes are less pronounced than normal. 

In cases where there were inequalities in the blood flow of two hands 
(through mechanical causes, ligation, embolism, compression) the stability 
of the ratio of the flow in successive measurements was found characterisic. 
Tests made at long intervals demonstrated the development of collateral 
circulation by changes in the ratio of the blood flow in the normal and affected 
parts. A feature diagnostic of the organic impairment of the circulation was 
found to be the impossibility of abolishing or greatly altering the flow by the 
artificial production of vasomotor changes (through external temperature). 
In other words, temporary vasomotor instability could be made to give differ¬ 
ent readings in an artificial way. 

Inequalities of blood flow in two hands or feet of the nature varying in 
degree from day to day, and such as could be abolished, produced, increased 
or reversed, by changing the external conditions, were interpreted as due to 
unequal activity of the vasomotor mechanism on the two sides. 

In 3 cases of Raynaud’s disease the hand flow was subnormal; in the more 
advanced cases very much below the normal. 

Stewart summarizes the application of his method as follows: 

“The arterial pressure is not in itself a measure of the flow. With a high pressure the 
flow may be small, with a relatively low arterial pressure it may be large. Indeed, in cases 
of marked arterial hypertension the blood flow in the extremities has been found subnormal, 
the high blood pressure being associated with constriction of peripheral vessels and under¬ 
irrigation of peripheral parts. If the brachial or femoral artery were obstructed by a clot 
(or a ligature) the pressure in the artery central to the block would be at least normal. 
But this would be of no consequence to the patient and would not give the physician any 
information in regard to the important question, how much blood was passing through the 
endangered part below the block. The same is true of more limited lesions involving one 
or both hands or feet, or portions of them. In a considerable group of pathological condi¬ 
tions in which the blood vessels of one or more extremities are involved either primarily 
or secondarily (thrombo-angiitis obliterans, Raynaud’s disease, thrombosis associated with 
the puerperal state, embolism, etc.) measurements of the blood flow from time to time may 
yield information of importance, not otherwise obtainable. 

In this way the physician may learn: (a) Whether the blood flow is so small that gan¬ 
grene is probably imminent, although it may not yet have declared itself. A blood flow 
around the critical level would, of course, emphasize the importance of sedulously protect¬ 
ing the part against mechanical injury or cooling. ( b) Whether the vascular condition 
is stationary, improving or growing worse, (c) The effect, if any, of therapeutic meas¬ 
ures (vasodilator drugs, baths, Bier’s bandage). In certain cases the diagnosis between a 
functional vasomotor affection and a mechanical block, due to embolism, thrombosis or 
anatomical narrowing of the vascular lumen, can be made by testing the effects of vaso¬ 
dilator drugs or changes of external temperature upon the blood flow. A mechanical 
block will obviously resist such measures, and the blood flow will remain small, while a 

1 Stewart, Harvey Lectures, 1912, p. 86 (Lippincott). 


PHYSIOLOGY OF THE PERIPHERAL CIRCULATION 


51 


functional (vasomotor) block may open up. In cases where it is proposed to tie an artery, 
information as to the probable adequacy of the collateral circulation immediately after 
ligation could sometimes be obtained with advantage before the operation by blood flow 
measurements with the artery compressed and open (Matas). In several cases in which the 
innominate and right carotid were tied for subclavian aneurism (Hamann) comparison of 
the flow in the two hands enabled the gradual establishment of the collateral circulation 
to be followed till it was adequate for the normal functioning of the right arm. In cases of 
injury to the nerves of a limb, especially unilateral injury, information of value in the 
diagnosis can sometimes be obtained by blood flow measurements, paralysis of the vaso- 
motors in the injured nerve trunks leading to definite changes. In early brachial neuritis, 
e.g., the flow in the corresponding hand is likely to be increased. Such measurements 
have aided in discriminating between pressure on the subclavian artery and injury to the 
brachial plexus as the cause of certain symptoms in the arm and hand.” 

“In the study of pathological conditions of the circulation in the extremi¬ 
ties it is sometimes useful not only to determine the rate of the blood flow, 
but also the degree in which it is affected reflexly through the vasomotor 
system. It is perhaps not too much to say that the proper application of 
reflex tests is as important in the investigation of diseased conditions of 
the vasomotor system as in the investigation of diseased conditions affect¬ 
ing the skeletal affections of the extremities. For, one of the most char¬ 
acteristic properties of the cutaneous circulation (and the circulation of 
the hands and feet is essentially cutaneous), is the variation in its rate accord¬ 
ing to the intensity of the metabolism and the temperature of the environ¬ 
ment. And this adjustment is brought about largely through vasomotor 
reflexes. 

The intensity of the vasomotor reflexes elicited by heat and cold can be 
estimated by immersing one hand or foot in cold or warm water, while the 
blood flow in the other is being measured. (A reflex vasoconstriction is 
associated with a diminished flow, a reflex vasodilatation with an increased 
flow. The reflex vasoconstriction to cold has been found intensified in 
cases of Raynaud’s disease and allied conditions, feeble or absent in tabes, 
in well marked arteriosclerosis, the in long-standing hemiplegia, etc.) It is 
obvious that where anatomical changes have occurred which constitute a 
block on the vasomotor reflex arcs, even without obstruction of the vascular 
path, or a block, on the vascular path, even without interference with the 
vasomotors, vascular reflexes must fail to affect the blood flow through the 
part.” 

The Blood Vessels and the Blood Movement.-—Two views regarding the 
role of the vascular system in the circulatory activity have found adherents in 
the literature. According to one of these the blood vessels take an active 
part in the propulsion of the blood. This presumes that the vessels pulsate 
actively, and propel the blood forward in a peristaltic wave, and this power 
is attributed not only to the arteries, but also to the veins. 

According to Hasebroek 1 the pulse wave occasioned by the heart stimu¬ 
lates first the vasodilators, so that an active dilatation of the arteries ensues. 
When the pulse waves have reached the maximum, a vasoconstricting effect 
is aroused, and an active constriction takes place. Inasmuch as the pulse 
wave is transmitted from place to place towards the periphery, this stimula¬ 
tion and motion of the arteries is believed to take the form of a peristaltic 
wave, so that the blood is, as it were, aspirated during the diastole of the 
arteries and transmitted onward during the systole. 

This view has not been acceptable to all investigators. Indeed, another 
school insists that the passive dilatation of vessels and the consequent re- 

1 Hasebroek, PfUiger’s Arch. Bd. 168, 1917, p. 247. 


52 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


bound, gives rise to the mistaken impression of spontaneous activity. These 
investigators, therefore, hold that the vessels play a passive role only. 

There seems to be no doubt, however, that the vessels are active so far as 
certain variations in their caliber do depend upon nervous influences. 
Through the vasomotor system the vessels conserve a certain degree of ten¬ 
sion or so-called tonus. 

Capillary Circulation and Blood Movement .—The capillaries are prone, to 
show ryhthmic contractility following nerve stimulation. This observation 
is of importance for its bearing on the existence of an extracardiac force 
in the propulsion of blood. Fleisch 1 contends that the rhythmic contractions 
exhibited by the excised arterial strip does not prove that an independent 
extracardiac propulsive force exists. 

This author calls attention to the fact that the rate of contraction of isolated arterial 
preparations at body temperature is less than the heart rate. If, therefore, such vascular 
movements occurred in the normal intact animal, they would be as likely to impede as to 
facilitate the force of the heart beat since they are neither synchronous with it, nor can they 
travel with the same rapidity over the vascular tube. He rejects the view, therefore, that 
the arteries furnish an extracardiac circulatory force. Whether the veins contribute 
circulatory power is still a mooted question. Since cinematographic records show.no rhyth¬ 
mic change of caliber in the capillaries, the latter are probably also impotent as circulatory 
adjuvants. 

Hooker takes exception to these views in the light of recent investigations. He states 
that the mammalian capillaries and venules have been shown to undergo post-mortem 
changes in that they are almost completely emptied of blood shortly after death. Later 
they fill again and subsequently and finally empty themselves. Since no extraneous forces 
are at work, this phenomenon cannot be passive in character both as to emptying and filling. 
In other words, the capillaries under these circumstances exhibit a functional response 
which might be of distinct moment in moving the blood under normal conditions. 

In accordance with more modern investigations, it does not appear unwarranted to 
entertain the view that the capillaries and venules may offer an extracardiac force of very 
considerable significance to the circulation. 

Hooker says that “ up to the present, no one has attempted to show, except in the case of 
the bat’s wing, that the veins proper facilitate blood movement by contractile activity 
There is abundant evidence that the tone of the veins is an important factor in circulatory 
regulation and we know that respiratory, joint and muscular movements facilitate, by a 
massage effect, the movement from valve segment to valve segment of the blood in the large 
veins. The sole indication, however, that the veins may move the blood by a kind of 
peristaltic activity is found in analogous observations that the large lymphatic trunks in 
situ may exhibit spontaneous rhythmicity of a peristaltic character.” 

Vasomotor Function and Circulation. —To understand better the action of 
the vasomotor nerves, let us quote the example given by Starling 2 of the 
effect of vasoconstriction and dilatation of the arterioles of a part or organ of 
the body. 

“If the arterioles A in the organ B dilate (Fig. 28), the first effect is a diminution of the 
resistance to the flow of blood into the capillaries beyond. Supposing that the arterial 
pressure in the trunk C remains constant, a local diminution of resistance in A will at once 
determine an increased flow of blood through the arterioles, and the fall of pressure from A 
to the capillaries will be less than when the arteriole was constricted. If the organ is 
distensible and elastic, the increased pressure in the arterioles and capillaries will cause 
dilatation of these vessels, and a consequent dilatation of the whole organ. The same 
effect on intracapillary pressure, and therefore on the volume of the part, may be caused 
by obstruction to the flow of blood from the veins. Provided that there is no obstruction to 
the flow of blood through the veins , and that the general blood pressure in Cremains constant, 
dilatation of an organ may be taken as an expression of vasodilatation in the arteries with 
which it is supplied. The diminution of the resistance in A may also increase the velocity 
of the flow through the part, since the amount of blood flowing in a given period of time 
through any vessel varies directly as the difference of pressure, and inversely as the resist¬ 
ance in the vessel.” 

1 Fleisch, Schweiz, med. Wchnschr., June 10, 1920, 323. 

? Starling, loc. cit., p. 989. 


PHYSIOLOGY OF THE PERIPHERAL CIRCULATION 


53 


Vasodilatation, therefore, leads to increased circulatory conditions and 
a heightened velocity of blood through the parts involved. Wherever, an 
increased demand for local blood supply occurs, a nervous mechanism is set 
into action with a view to enhancing the circulation. So also an increased 
blood pressure will cause vasodilatation. 



If we compare these physiological observations with the phenomenon of 
erythromelia described under thrombo-angiitis obliterans and arteriosclerosis, 
we will appreciate how an increase of blood pressure or greater demand for 
capacity is made on the superficial arterioles. For with so many of the deep 
circulatory avenues occluded and with the diminished influx to the muscles and 
profound parts, the tendency to fill the superficial arterioles and capillaries by 
way of collaterals or paths still uninvolved, must be increased. And with the 
rise in local pressure, an inducement to arterial expansion is at hand. To 
what extent neurogenic vasodilatation is responsible is not known. 

The Vasomotor and Autonomic Responses. —A large number of observa¬ 
tions tend to show that after a transitory contraction, the capillaries are prone 
to dilate upon the action of cold. Nagelsbach 1 observed that when the hand 
is put into snow, reactive dilatation of the capillaries can be observed with the 
Weiss 2 method. This author found the capillaries dilated and the circulation 
retarded as a result of the action of the snow compress, the color of the fingers 
becoming bluish, continuing so during a five minute period of observation. 
After the removal of the snow and drying of the fingers, the altered color and 
the dilatory circulation persisted about five minutes before the return to 
normal took place. 

The dilatation of the capillaries following the action of the cold is regarded 
as a reactive process similar to that seen in acute inflammation and in the 
hyperemic reactions after the applications of a tourniquet. A similar 
phenomenon, elsewhere described as a reactive or reactionary or induced 
hyperemia or erythromelia, is noteworthy in organic vascular diseases, espe¬ 
cially in thrombo-angiitis obliterans. Some believe that the dilatation of the 
capillaries may, however, be due to the direct action of the cold upon the 
vessel muscle. 

1 Nagelsbach, Deutsch. Ztschr. f. Chir., 160, 1920, p. 221. 

2 Weiss, Ztschr. f. exper. Path. u. Therap., 1918, Bd. 19, p. 390. Described in Chap. 
VIII. 



























54 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Such reactionary conditions may occur without participation of the spinal 
nerves. Bier has shown that they manifest themselves in an extremity 
that has been wholly cut off from the trunk experimentally, a glass tube 
bridging the gap and providing for continuity of arterial circulation. 

That the vessel nerves are not essential is deducible from the experiments 
of Lewarchew 1 who was able to obtain reactions in the vessels even after the 
electrical irritability of the cut nerve had been exhausted. It is hardly 
extraordinary that such independent function of the muscle fibers of the 
vessels exists, since the embryonic parts of certain animals are seen to contract 
before nerves have been developed. We may concede, therefore, that the 
reaction of the vessels through cold does not necessarily take place by way of 
nerve paths. This response in the vessels can be strengthened by adaptation 
to climatic conditions. The reactionary rubor in thrombo-angiitis obliterans 
is another beautiful example of adaptation of circulatory conditions to a new 
status, and also can be observed to develop as it were, under our eyes, namely, 
during the period of clinical observation. 

The secondary vasodilatation after preliminary vasoconstriction that 
results from the action of cold, seems to be of teleological significance, since 
nourishment of the affected part is furthered by the increased flow of blood. 
These phenomena seem to occur most rapidly and most intensively in the 
exposed portions of the body. The dilatation of the capillaries diminishes 
the resistance in the affected territories, whilst the dilatation of the afferent 
arteries makes possible the delivery of a larger quantity of blood. Thus, 
the enhancement of the circulation adds calories to the parts, whilst the 
flowing of the capillary stream by virtue of their dilatation enables a larger 
distribution of calories to take place in the tissues. The added warmth thus 
acquired can be so intensive that a limb dipped in ice water may lose no more 
than .2° C. after almost an hour’s exposure. 

In anemic individuals the reaction is deficient. In keeping with this 
observation is the fact that anemic individuals are more apt to suffer from 
frost-bite. Bier has observed that in such individuals it is difficult to produce 
the typical red form of stasis (hyperemia) or congestion upon the application 
of the elastic bandage. 

The changes in the tonicity of the vessels is partly of reflex origin, and so 
remote actions may be produced. When one arm is plunged into cold water, 
the cutaneous vessels of the other arm may undergo constriction; and indeed, 
with even a similar but less marked reaction over other parts. This phe¬ 
nomenon has been employed by physiologists (Stewart) in studies of blood 
movement in the extremities, and is often invoked as an index of the sus¬ 
ceptibility of the vascular system to vasomotor reflexes. 

The Chemical Regulation of the Blood Vessels.—Substances called meta¬ 
bolites produced incident to katabolic activity, may chemically stimulate 
the vessels themselves and increase the blood flow. Krogh believes that there 
is normally a hormone, possibly derived from pituitary function, that brings 
about a certain degree of tone in the capillaries. Here we are concerned, 
however, with the larger vessels. 

The great enhancement of the flow through the muscles associated with 
muscular exercise is brought about largely by overactivity. The experi¬ 
mental introduction of carbon dioxide or lactic acid into the blood causes 
marked dilatation of the blood vessels of a limb. Carbon dioxide then, 
regarded as a universal hormone liberated in the circulation on general 

lewarchew, Pfluger’s Arch., 1881, Bd. 26, p. 60. 


PHYSIOLOGY OF THE PERIPHERAL CIRCULATION 


55 


increase of body activity, seems to have not only a central effect through 
excitation of the medullary and spinal centers (causing contraction of the 
blood vessels), but also a local peripheral effect bringing about vascular 
dilatation. The total result therefore, according to Starling would be “to 
cause dilatation of the blood vessels of the part when carbon dioxide is pro¬ 
duced, and where it is present in greatest concentration, and vascular con¬ 
striction elsewhere under the influence of the sensitive nervous system.” 

How such physiological processes are deranged, can be exemplified by the 
ischemia that is often noted after exertion in the foot and legs of cases of 
arteriosclerotic disease and thrombo-angiitis obliterans. Such blanching 
is diametrically opposed to the functional regional demands and to the modus 
above described. Whether we are to presuppose a heightened irritability of 
the vasoconstrictor centers whose actions nullify the local tendency to arte¬ 
rial expansion produced by the carbon dioxide, or whether by reason of 
impoverished local circulation, other chemical agents counteract the expected 
and usual phenomena, are questions that have not as yet been solved or 
satisfactorily answered. 

The products of tissue activity are also believed to exercise an influence 
on the caliber of the arterioles. Gaskell demonstrated that acids (especially 
lactic) may have a direct action on the arterioles, causing these to relax. 
Bayliss found that carbon dioxide produces a like effect. Both the latter 
and lactic acid result from processes of oxidation, carbon dioxide in all cellu¬ 
lar activity, lactic acid usually in muscle. Bayliss concludes that carbon 
dioxide may be one of the chief chemical agents capable of bringing about 
increased blood supply to active tissues. However, the action of “metabo¬ 
lites” is in all probability aided by vasodilator nervous reflexes. 

The Internal Secretions and the Circulation. —The endocrine glands have 
a double relation to the vegetative nervous system; and the regulation of 
their secretory activity is believed to be dominated by the vegetative paths 
in spite of the fact that the glands may functionate when all afferent nerves 
have been divided. Then, too, the hormones delivered into the blood paths 
may modify the excitability of the vegetative nervous system. 

For example, the adrenals receive secretory fibers from the splanchnic; and adrenalin on 
the other hand, may stimulate, the sympathetic nerve endings, and in turn enhance the 
secretory activity of these glands. 

Authors are not in accord regarding the influence of the thyroid secretion 
on the vegetative nerves. It probably exercises a stimulating effect upon the 
sympathetic and parasympathetic fibers. 

It may suffice here to refer briefly to the latest theories regarding the 
action of adrenalin , the hypophysis and the pituitary bodies. 

Adrenalin .—The constrictor effect of adrenalin on the small arteries, 
arterioles, capillaries and portal veins with the consequent increase in 
arterial blood pressure is well-known. This contraction has been observed 
after section of the cervical cord, and destruction of the spinal cord, and 
therefore has been interpreted as an influence acting directly upon the 
vascular musculature. The vasomotor centers, however, are regarded as 
playing a role by some. Although physiological observations would indi¬ 
cate that the normal vessel tone is dependent upon the direct action of 
adrenalin, this view is not in accord with the circumstance that the adrenalin 
action disappears rapidly; nor is it in consonance with the failure of the 
blood pressure to fall after bilateral exclusion of the adienal bodies. And 
so others take the view that adrenalin under normal conditions conserves 


56 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the receptivity of the vessel musculature to stimuli brought to it from the 
central nervous system. Still others believe that under excessive demands, 
an abnormal amount of adrenalin is given off, and the vessel muscle is directly 
irritated by this internal secretion. Under such circumstances the adrenal 
bodies play an important role in the regulation of the vascular tone. 

The question as to whether adrenin contributes under normal condi¬ 
tions, in the maintenance of the blood vessel tonus has given rise to much 
discussion. Although many believe that this substance is continually 
present in the blood and is a factor in the maintenance of the tonus of the 
blood vessels, Hoskins , 1 Vincent , 2 and Stewart 3 are not in accord with this 
view. 

These investigators have been unable to find adrenin in the blood stream. 
Furthermore, under normal physiological conditions, they believe that it has 
no effect on the physiologic processes. Under special strain, however, when 
the sympathetics are stimulated, the chromophil cells of the medulla of the 
adrenals are stimulated and adrenin is thrown into the blood steam. Under 
these conditions it may intensify and prolong the sympathetic action. 

Adrenin may not always produce vasoconstriction as is generally believed. 
Its effect depends upon its‘concentration and dosage; and it may produce 
vasoconstriction in one set of vessels and compensatory vasodilatation in 
others. 

Hartman 4 states that the mechanism causing vasodilatation in the intestine, when 
adrenalin is injected into the general circulation, is located in the collateral sympathetic 
ganglia, probably in the superior mesenteric ganglion. He further believes that “in the 
adult, adrenalin poured into the blood in small quantities, causes by its peripheral effects, 
constriction of the vessels in the skin, mucous membranes, and abdominal organs, driving 
the blood into the vessels supplying the skeletal muscles which are actively dilated for its 
reception through the effect on the sympathetic and dorsal root ganglia mechanism. But 
as the quantity of adrenalin liberated increases, the peripheral effect begins to overcome the 
gangliar effect in skeletal muscles, the intestinal vessels by action on the sympathetic ganglia 
begin to dilate and the blood is reversed in its path.” 

The role of adrenalin with respect to its influence on the regulatory vegeta¬ 
tive mechanism in the corpus striatum and mid-brain (Dresel-Brugsch) is 
given more detailed consideration elsewhere (Chapter on Vasomotor Neuroses). 

The hypophysis cerebri is also believed to have an influence on the circula¬ 
tion. A colloid substance is formed in its middle portion, which is said 
to extend and permeate through the infundibulum into the third ventricle. 
According to Schaffer two substances can be extracted out of the hypophysis, 
and these differ chemically. One of these produces a transitory fall of 
arterial pressure. The other substance is pituitrin, which can be extracted 
from the human hypophysis, and which causes retardation of the heart 
action. All vessels of the body, even those of the lungs and the heart may be 
caused to contract by the action of pituitrin. Only the vessels of the kidney 
are an exception, for these may even dilate. The action of pituitrin as a 
vasoconstrictor is more durable than that of adrenalin; but after repeated 
injections its effect diminishes, and may at times bring about a reduction in 
the blood pressure. Inasmuch as the action of pituitrin continues even 
after destruction of the higher vasomotor centers, it probably has a direct 
influence upon the peripheral vascular mechanism. 

It has been recently suggested that the blood contains a substance 
essential for the maintenance of the contractility of the Rouget cells—those 

1 Hoskins, Endocrinology, i, 292. 3 Stewart, Endocrinology, 1, 151. 

2 Vincent, Endocrinology, 1, 140. 4 Hartman, Endocrinology, 1918, 2, p. 1. 


PHYSIOLOGY OF THE CAPILLARIES 


57 


elsewhere described as responsible for inherent capillary activity. Experi¬ 
ments (Krogh and Rehberg) have sought to identify this substance with 
the pituitary hormone. Indeed, preponderating evidence is in favor of 
the existence of such a hormone that may act in a dilution equal to i :ioo,ooo, 
or 1:1,000,000 of commercial pituitrin. 1 When circulating in the blood, a 
physiological effect is doubtless exercised on the capillaries. In view of 
the discrepancies in the action of pituitrin on various vessels of animals, 
much clarification of our present knowledge on the mechanism of capillary 
tonus is still desirable. 


CHAPTER VII 

PHYSIOLOGY OF THE CAPILLARIES 2 

General Considerations.—For an understanding of the visible mani¬ 
festations of changes in arterioles and capillaries in deranged circulation 
of the extremities, it is well to review certain elementary facts regarding 
capillary circulation. 

1. The total number and volume of the capillaries is enormous as com¬ 
pared to that of the arterioles. 

2. The rate of flow is greater in the arterioles than in the capillaries. 

3. Pressure on the arterial side must needs be markedly increased when¬ 
ever the caliber of the arterioles becomes diminished; for here the flow is 
rapid and friction is proportionate to velocity. 

4. The importance of variations in size of the capillaries can be well 
understood if we consider that but slight dilatation over a large area may 
cause accumulation of a large amount of blood. 

Recent observations in the normal state of the capillaries and their 
responses to various stimuli are illuminating and open a new vista of thought 
in explanation of signs of obstructed peripheral circulation. 

Normally, a relatively small number of capillaries in the muscles is filled 
with blood (Krogh). Muscular activity alone suffices for the dilatation of 
the collapsed capillaries. Nature would not adequately play her role did 
not the arterioles, too, enlarge commensurately. For, with dilatation of 
capillaries alone , the total blood supply would be hardly augmented, and 
stasis in the dilated capillaries with defective oxygenation occurs. With 
contracted arterioles the stagnation would be intensified. 

From these physiological facts we would infer that a disharmony in the 
reciprocal functional activities of arterioles and capillaries may be responsible 
for some of the clinical evidences of disturbed cutaneous circulation. 

But an independent activity of the capillaries plays an important part 
both under normal and pathological conditions. Whilst the arterioles may 
contract synchronously with the capillaries as upon the action of cold, 
they may manifest opposite motility. 

When the skin is hyperemic, red and warm, the flow through the capil¬ 
laries is enhanced and the arterioles are simultaneously dilated. This is a 
defense mechanism of nature against cold and other insults. 

When the skin is cyanotic or bluish, it is usually cold, the supply of 
blood impaired, oxygenation diminished and the current of blood retarded. 

1 Parke, Davis & Co., pituitrin from the posterior portion of the pituitary. 

2 For deductions based on capillary microscopy the reader is referred to Chap. CVI. 



58 . CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

Here we must assume opposed activities—the arterioles constricted, the 
capillaries open or dilated. It is conceded to-day that these structures are 
capable of active alterations in caliber. 

The fact that capillaries consist of but a single layer of protoplasmic 
cells and are devoid of a muscular coat does not preclude active changes in 
their caliber, since we know that cells other than muscle can undergo altera¬ 
tions in form under stimulation. More recently, however, powers of con¬ 
tractility have been relegated to certain other elements in the capillary 
walls (Vimtrup and Krogh). Rouget in 1873 described strongly branched 
contractile cells lying on the outside of the endothelial walls, sometimes 
almost completely encircling the capillaries. Latterly it has been shown 
that the contraction of capillaries begins at one or more of these cells. Their 
function is believed to be that of altering the lumina. 

The Autonomic Action of the Capillaries. —Clinical observations on the 
variations in color tints that may occur in many of the neurogenic forms of 
the vascular maladies have often aroused the doubt that pathologic nerve 
impulses alone could explain the phenomena. Let us recall the evanescent 
mottling of red, white and bluish black that may come and go in certain 
cases of thrombo-angiitis obliterans, particularly when the affected part is 
unclothed in a warm room after exposure to the cold; and let us call attention 
to the play of colors and the variegated mottling in patches of indeterminate 
shape and size that are characteristic manifestations in some of the cases of 
vasomotor instability and Raynaud’s disease. Such multiform evidences 
of capillary activity or passivity, corresponding to no known areas of vascular 
or even nerve distribution, have oft awakened the thought that neither purely 
mechanical, obstructive or neurogenic influences offer adequate explanation. 

Leaving out of consideration the role of the pumping mechanism, and 
reviewing the peripheral factors in the blood vessels themselves, we have 
been taught that vasomotor influences are for the most part responsible for 
the alteration in peripheral resistance, and the quantitative distribution of the 
blood into the tissues. Physiologists have relegated the functional vessel 
control to the vasoconstrictor and vasodilator nerves that are said to act in 
the arteriole walls. It has been conceded, too, that because of a certain 
sensitiveness on the part of the vessels and the products of cellular activity, 
and possibly exogenous toxins too, local vascular changes in volume might be 
the result of the action of metabolites and hence not be altogether dependent 
on nerve control. Hooker, 1 believes that capillaries can dilate or contract 
independently of the larger vessels with which they are continuous. The 
capillaries and venules are thus regarded as able to furnish peripheral resis¬ 
tance as well as the arterioles. Hooker concedes the role of chemical factors 
as influencing the peripheral circulation. He thinks that, as a rule, there is a 
harmonious interrelation of the activity of the higher nervous control and 
the primordial autonomic (possibly chemical) regulated forces possessed by 
the smallest vessels. 

For an understanding of this more modern view regarding the activities 
of the capillaries and their responses to both nerve and local chemical influ¬ 
ences , some of the observations and researches that have led up to the 
acceptance of autonomic activity may be worthy of mention. 

The facts that have been experimentally adduced may be summarized as 
relative to: 

1. Nerve control of capillaries and venules; and 


1 Hooker, Am. Jour. Physiol., 54, 30, Nov. 1, 1920. 


PHYSIOLOGY OF THE CAPILLARIES 


59 


2. Direct influences on capillaries, arterioles and venules. This second 
group of possible motivating agents is again divisible into 

(a) Direct mechanical stimuli; and 

(b) Direct chemical (metabolic, katabolic) stimuli. 

The clinical data in support of the newer concepts will be discussed 
separately wherever the diseases or manifestations of deranged peripheral 
vascular function seem to have a bearing on the hypotheses here expressed. 

i. The Nerve Control of the Capillary Circulation. —In the theory of 
capillary function, the effect produced by nerve stimulation is the cardinal 
factor. Sectioning and stimulating the cervical sympathetic in the cat 
produce at first a cessation of corpuscular flow, due in all probability to 
arteriolar constriction. The corpuscles then begin to clump and move for¬ 
ward in an irregular fashion, so that in the relatively brief time that the 
electrical stimulus is continued, the corpuscles disappear from the field of 
observation. Immediately after cessation of the stimulus, however, the 
appearance of corpuscles from the arterial side is again noted in more profuse 
flow than before. This phenomenon can be obtained successively on the 
same preparation without any indication of fatigue, evincing conclusively 
that the capillaries and venules are subject to nervous control. 

Still other experiments (Krogh) on the capillary responses to punctiform 
trauma of the frog’s tongue have demonstrated that stimulation of sensory 
nerve filaments may result in capillary dilatation; and this by way of a 
sensory vasomotor nerve reflex in an antidromic direction. 

It is generally conceded to-day that epinephrin acts only on tissues with 
sympathetic innervation. If 3 cc. of a 1150,000 adrenalin solution be injected 
intravenously, the action of the capillary bed is similar to that in nerve 
stimulation, in that there is a cessation of the corpuscles, clumping, with 
gradual and irregular movement out of the field. It may be accepted then 
that the observations here described are directly dependent upon a functional 
response of the endothelium. 

Recent observations also point to a regulatory nerve mechanism in the 
case of the veins. 

Peripheral Venopressor Mechanism. —Venous pressure may be caused to rise 1 in the 
sigmoidal area of the large intestines in dogs, isolated except for its nervous connections 
via the inferior mesenteric ganglion. After washing out the blood by perfusion, the artery 
was left open and the drainage vein connected with a water manometer. A rise of pressure 
of 7.5 cm. of water followed direct electrical stimulation of the nerve to the part; 
indirect stimulation (asphyxiation) acting by way of the medulla gave a rise of 4.5 cm. of 
water. A possible action of the intestinal musculature was excluded by coincident records 
of the pressure within the lumen of the gut itself. Hooker records as follows “the results 
thus obtained were regarded as substantiating the existence of a central as well as a periph¬ 
eral venopressor mechanism. Whether the contraction was in the larger vein, in the 
venule or in the capillary, or in all of them together, was not possible of determination, but 
it was believed that the ateriole and artery were effectively excluded. In our present 
knowledge we should probably emphasize the participation of the capillary and venule 
although the direct evidence is not at hand in this particular experiment.” 

Briscoe 2 made a careful study of the venous and capillary pressures in the cyanosis of 
the hands associated with “irritable heart.” A special apparatus was used; with it the 
collapse of the superficial veins was regarded as criterion for venous pressure, and the 
blanching of the skin under the glass capsule as indicative of capillary pressure. Through¬ 
out the observations the venous pressure was found within normal limits (average 11.4 cm. 
H 2 0 ). The capillary pressure was, however, uniformly high and sometimes as high as 
twice the normal. The average capillary pressure for the controls was 23.5 cm. H 2 0 , and 
for the subjects with well marked blue hands 36.9 cm. H 2 0 . In these cases there is little 
doubt of capillary stagnation; the blue color, the tendency to perspire, the dark color of the 

1 Hooker, Am. Jour. Physiol., 1918, XLVI, 91. 

2 Briscoe, Heart, 1918, VII, 35. 


60 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

blood, which exudes from a skin prick, all point to this condition. She states that the stasis 
might be due to arteriolar constriction; but that this factor may be excluded on the ground 
that the capillary pressure is too high. The only mechanism which could develop such high 
capillary pressures with an engorgement accompanied by a normal venous pressure , would be 
a constriction of the venules, and this is the explanation which Briscoe proposes. . 

The Sympathetic Innervation of the Capillaries. —Since electrical stimulation of the cervical 
sympathetic is followed by marked constriction of the capillaries in the skin ot the cat s 
ear (Hooker); and in light of similar effects in the capillaries of the frog s web after excita¬ 
tion of the lower sympathetic ganglia (Krogh, Harrop, Rehberg), the influence of the 
sympathetic nerve mechanism has been definitely proven. Indeed, contractions are 
believed to start from the sites of the nuclei of the capillary contractile cells (Rouget). 
the latter being probably directly supplied by nerve fibers. 

2. The Direct Response of the Capillaries, (a). To Mechanical Stimuli — 
Cotton, Slade and Lewis 1 in a study of the subject of dermatographia as 
exhibited in soldiers with “irritable heart,” showed that some of the condi¬ 
tions observed seem attributable to a contractile function of the capillaries. 
They regard the red line of the tache and the flush, which may surround it, 
as due to arteriolar dilatation which floods more blood into the capillary bed. 
The white tache and the white area beside a red tache, however, are believed 
due to capillary constriction. 

The spontaneous activities of the capillaries are most clearly attested by 
those experiments in which the blood flow in an arm was completely shut off 
by a supra-systolic pressure in a sphygmomanometer cuff. With the cardiac 
factor thus excluded and with the arm held horizontally at the time this 
pressure was applied, the color of the skin remained normal and the stroke of 
a blunt instrument developed a white tache just as distinct as under normal 
circulatory conditions. 

Since this reaction could be obtained at any time during io minutes of applied pressure, 
Cotton and Slade assume a stabilized pressure in the vessels. If under such circumstances 
the capillaries empty themselves of blood on appropriate stimulation, the result cannot be 
ascribed to arteriolar constriction and must be due to a response on the part of the capil¬ 
laries themselves. Under the same conditions stronger mechanical stimulation of the skin 
produced a red tache which was assumed to be due to a capillary dilatation, thereby per¬ 
mitting blood to enter from the larger neighboring vessels. 

Employing the same procedure and with the larger channels compressed, these authors 
found that the cutaneous injection of a few drops of 1130,000 adrenalin causes a localized 
pallor, much as is the case when the substance is injected with circulation intact. With 
the blood flow in the large vessels shut off, the pallor is said to be due to an effect exerted 
upon the capillaries directly. 

(b). To Chemical Stimuli. —Krogh 2 states that in the resting muscle many 
capillary channels are occluded; and that following activity the number of 
patent capillaries is enormously increased. The katabolic products of muscu¬ 
lar activity are responsible for this capillary response. This author points 
out how fallacious is the older view that “the number of functioning capil¬ 
laries in any tissue depends upon the tension of blood in the arterioles, and 
that as this tension rises more and more, capillaries open up as if their tonicity 
varied in degree from capillary to capillary.” For if this were so, the blood 
would tend to follow certain fixed paths when the pressure was low, and as a 
result, some cells would be well supplied with oxygen, while others would be 
in constant danger of suffering oxygen want. According to the recent views 3 
the capillaries are susceptible to chemical stimulation; and the blood 
may be deflected from one set of channels to another according to the tissue 
needs of their environmental cells, without changes in arteriolar pressure. 

1 Cotton, Slade and Lewis, Heart, 1917, VI, 227. 

2 Krogh, Jour. Physiol., 1919, LII, 409. 

3 Hooker, Loc. cit. 


PHYSIOLOGY OF THE CAPILLARIES 


61 


Danzer and Hooker 1 found “that one of the annoyances in determinations of capillary 
blood pressure in man, when the criterion employed was the cessation of corpuscular flow, 
lay in the fact that often the large and conspicuous capillaries were filled with stagnated 
corpuscles, and they noted that in the course of observations it was not uncommon to find 
that a previously stagnated vessel had become patent and that on the other hand, patent 
vessels became stagnated. Furthermore, they found under varying experimental condi- 
tions that the pressure might rise or fall in one capillary while the pressure in its neighbor 
remained constant or changed in an opposite direction. The structural conditions of the 
vascular bed are undoubtedly such that in the vast majority of instances neighboring 
capillaries are supplied by the same arteriole. Variations in neighboring capillaries such 
as have been noted, therefore must be due to inherent and independent changes in the 
vessels themselves.” Perhaps many of the so-called vasomotor phenomena in organic 
vascular disease can be also thus explained. 

Krogh states that capillary tone is not only independent of the blood pressure but that 
the spreading of the effects of stimuli is due to axon reflexes which are probably conveyed 
along sensory fibers. This view is in accord with the conception of Bruce 2 and of Bardy 3 
that inflammatory processes resulting from the application of local irritants are essentially 
due to axon reflexes. According to Krogh the capillary tonus is not of nervous origin, 
but must depend upon some constituent of the blood, and this constituent is not oxygen. 

Paralytic Action of Poisons on the Capillaries. —Heubner 4 has shown that the intraven¬ 
ous injection of the double chloride of gold and sodium produces a shock-like prostration 
accompanied by a remarkable engorgement and stasis of the capillaries and veins. Post¬ 
mortem examination in the case of mammals showed distended and conspicuous veins which 
could be traced as fine twigs to the surface of the intestine. The peritoneal surfaces were 
injected, and a similar hyperemic appearance of the mucous membrane was noted. Micro¬ 
scopically all the tissue exhibited extensive dilatation of the venules and capillaries, and not 
infrequently ecchymotic areas. The small arteries everywhere were strongly contracted, 
usually with completely occluded lumina. 

Dale, theoretically and experimentally reached the conclusion without observation of 
the vessels concerned, that histamine is a capillary poison producing an effect upon the 
general circulation analogous to that established by the injection of gold salts. Cannon 5 
had previously presented evidence that the capillaries are packed with red cells in wound 
shock, and postulated this condition of “exemia” as the causative factor in the condition. 
This conclusion Rich 6 and Hooker 7 confirmed. Rich developed a method by which instant 
fixation of the omental tissues in situ could be obtained. He was then able to study the 
vascular picture microscopically after the omentum had been removed and spread upon a 
slide. Preparations made in this manner at various times after the intravenous injection 
of histamine in cats, and controlled by specimens in which physiological salt solution was 
injected, gave clear evidence that an immediate effect of the histamine was to greatly 
increase the number and size of the capillaries. 

In photographs of the capillaries of the cat’s ear, Hooker has shown that histamine 
causes a profound dilatation of the capillaries and venules. Though the latter believes that 
the vessels of this area may be less sensitive than in the omentum, he frequently observed 
that the dilatation due to histamine was preceded by a period of constriction. This 
constriction was usually fleeting in character, and while of considerable moment in regard 
to capillary function, is not to be regarded as disputing the hypothesis of histamine action 
under discussion. 

Histamine does not abolish arterial vasoconstriction upon sensory nerve stimulation. 
It does, however, completely depress the response of the capillaries and venules to 
peripheral nerve stimulation, indicating again its potency as a poison for the capillary 
endothelium. 

Summary of the Function of the Capillaries.—The significance of a 
thorough knowledge of the functions of the capillaries in the extremities will 
be appreciated when we recall that they are still patent when large vascular 
territories are occluded; that, though collaterals may step in to substitute 
for the large channels, the capillaries are essential for the delivery of oxygen 

1 Danzer and Hooker, Am. Jour. Physiol., 1920, LIV, 96. 

2 Bruce, Quart. Jour. Exper. Physiol., 1913, VI, 339. 

3 Bardy, Skandinav. Arch. f. Physiol., 1915, XXXII, 198. 

4 Heubner, Arch. f. exper. Path. u. Pharm., 1907, LVI, 370. 

5 Cannon, Jour. Am. Med. Assn., 1918, LXX, 611. 

6 Rich, Jour. Exper. Med. 

7 Hooker, Am. Jour. Physiol., 1920, LIV, 30. 


62 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


and nutritional elements, as well as for the transportation of the waste meta¬ 
bolites, and that functional impairment of these, too, may bring about 
morbid processes. 

The preponderance of evidence today, leans to the view that the capil¬ 
laries are not merely passive agents in which the blood flow is determined by 
the state of the supplying arterioles and the vessels that drain them. On the 
contrary, an inherent power of contractility and dilatability that actively 
influences the distribution of blood, is assumed to exist. 

Indeed, it has been suggested 1 that paralysis of the capillaries with consequent dilatation 
and stagnation of blood is demonstrable in “shock.” Hooker has shown that histamine 
produces a similar paralytic action upon the capillaries. Small doses, when injected, pro¬ 
duce a rise in blood pressure due to the contraction of the small arterioles. With larger 
doses, a primary rise in blood pressure soon yields to a marked fall with a consequent 
condition resembling ‘‘ shock. ’ ’ This is seen to be due to the fact that the capillaries become 
paralyzed and dilated with stagnation within them, thus rendering the arteriole contractions 
ineffective. 

To what extent the functional derangement of the capillaries is a factor in 
nutritional disturbances accompanying the obstructive and neurogenic vascu¬ 
lar affections of the extremities, is still a matter of conjecture . 

The capillary bed can adapt itself to local tissue needs by dilatation 
when tissue conditions tend toward asphyxiation, by constriction when such 
local needs have been satisfied. The mechanical alterations in the surround¬ 
ing tissue produces a variety of fluctuations in the girth of the capillaries. 
The corpuscles disappear from the capillary lumen when the capillaries con¬ 
tract and, per contra, the cutaneous capillaries may be overfilled With these 
elements. 

It may be admitted then, in the present state of our knowledge, that both 
chemical and nervous influences may regulate the activity of the capillaries. 
For the nervous mechanism constricting effects have been observed; and, in 
animal experimentation, sensory, vasomotor, antidromic reflexes causing 
dilatation follow trauma. 2 Chemical factors are said to bring about dilata¬ 
tion of the capillaries and venules. Perhaps then in consonance with the 
altered chemical constituents of the surrounding fluids and tissues, and with 
the exigencies of special metabolic stresses, a mechanism is at hand which 
automatically meets local demands. Hooker, therefore, believes that we 
may regard the nervous control as a force tending to restrict the capillary 
beds over the body as a whole, thus maintaining a tone which is played 
upon by chemical factors. 

Furthermore, since he accepts the existence of capillary and venule function in areas 
beyond that of the distribution of the arterioles, we must modify our conception of 
peripheral resistance, which heretofore had been restricted to the arterioles, the latter 
governed by nervous and chemical influences. 

In the case of the venules also, recent investigations have brought to light data that 
speak strongly in favor of independent functional activities. Some of the clinical confirma¬ 
tory evidences will be described later. Studies of the peripheral asphyxias would also seem 
to furnish corroborative testimony. 

Although much has been written regarding the vasodilating effects of 
acid metabolites in active organs, more recent authors do not accept the con¬ 
clusion that increased blood supply is due either in main or exclusively to 
the action of such metabolites. It is conceded, however, that metabolic 
products resulting from activity have a dilator effect upon capillaries, even 
though the action is not dependent on their acid properties. 

1 Dale and Cannon, Hooker, Physiol. Reviews, i, 112, 1921. 

2 See Chap. V. Recent Views on Physiology. 


METHODS OF INVEST IGA TING CAPILLARY CIRCULATION 


63 


The exact role of adrenalin in the maintenance of capillary tonus is still 
a matter of discussion; some ascribe an important part to this internal secre¬ 
tion (Dale and Richards), whereas others (Krogh) see in the pituitary 
activities the source of tonic influences for the capillaries. 


CHAPTER VIII 

METHODS OF INVESTIGATING CAPILLARY CIRCULATION 1 

Although the capillary territory occupies the longest part of the circula¬ 
tion time, relatively little is known about capillary dynamics. It is true 
that the hydraulic principles, by virtue of the implication of many other 
coefficients, can hardly be wholly accountable for the flow and its aberrant 
clinical manifestations. And so, in estimating the several factors that are 
determinants of capillary flow exclusive of the cardiac pump and general 
vascular tone, we must take into consideration the important roles that 
osmosis, absorption, cellular activity, and surface tension may play in this 
territory. 

The Lombard Method. —Lombard described a method of studying the 
human capillaries directly under a microscope. He applies a drop of gly¬ 
cerin or castor oil to the skin, and then observes this area through a micro¬ 
scope with a magnification of about 75 diameters. The capillary loops in the 
skin can be readily visualized and studied with a strong light thrown upon the 
area to be examined. The capillaries are seen as comma-shaped loops but 
the circulation within them escapes closer observation. At the base of the 
finger-nail or toe-nail, where the papillae of the skin are flattened out, they 
appear as long, horizontal, hair-pin shaped loops, in which the blood flow 
can be observed. 

Our investigations may take these directions all with a view to estimating 
capillary circulation; (1) the study of the morphology of the capillaries; 
(2) the character of the blood flow; and (3), the appraisal of the blood pressure 
within the capillaries by means of special instruments (Danzer and Hooker). 

The last is a small transparent air-chamber connected with a mercury manometer, by 
means of which pressure can be exerted on the skin, while the capillaries are kept under 
observation through the microscope. According to Boas the pressure is at first raised to 
the point at which the capillary flow ceases; and the reading is made at the point at which 
the capillary flow reappears after release of this pressure. 

We may briefly quote from these authors as to their observations in a 
field that promises much, rather in a prognostic than in a diagnostic way. 
Perhaps, however, certain criteria will be deduced from future investiga¬ 
tions that may be of service in differentiating the vasomotor vascular neuro¬ 
ses from those early cases of obstructive vascular disease of the extremities, 
that are at times difficult to recognize. 2 

Fluctuations under varying pressures are then recorded as the circulation 
is intermittently arrested. The figures given are, pressure of 60 to 70 mm. 
for the small arteries, 15 to 20 mm. for the small surface veins, and the ave¬ 
rage for the capillaries 40 mm. Allbutt quotes von Kries as finding lower 

1 For more recent work on this subject “Capillary Microscopy” see Chap. CVI. 

2 See Chap. CIV (Borderline Cases). 



64 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


estimates, as, for instance, 20 to 30 mm. of mercury in the capillaries. A 
reduction must needs occur in the smallest capillaries, and the above findings 
may represent rather the values in the intermediate arterioles. And so, 10 to 
20 mm. is regarded by many as being more accurate. 

The Miiller-Weiss Method— Most interesting data can be obtained if 
we study the capillary circulation in accessible parts of the fingers, with 
proper illumination and magnification. The horizontally placed capillary 
loops at the base of the finger nails, according to Muller and Weiss 1 give valu¬ 
able and interesting information concerning normal and pathological capillary 
flow. 

The finger of the case to be observed is placed under the microscope, the 
region just proximal to the root of the nail being selected. The area imme¬ 
diately under the lens is covered with a drop of cedar oil that also fills out the 
nail furrow. Observation is made with the Leitz objective A, or a Leitz 
objective No. Ill (occular No. 2 with about 40 diameters enlargement). 
The source of illumination is a strong electric lamp with a central illuminating 
filament (about 200 c.p.), whose light is thrown upon the object with a 
convex lens. 

When the capillary layer and epidermis pass over into the subungual space gradually, 
the capillary loops are more or less horizontally placed and easy to observe. However, if 
the epidermis makes a steep decline under the nail, annoying light reflexes are apt to take 
place which can be obviated to a certain extent if a cover slip is placed over the area covered 
with oil immersion. 

Under normal conditions the flow in the capillaries is rapid, continuous, 
and quicker in the arterial than in the venous limbs of the loops. The little 
experienced observer may have difficulty in recognizing the flow because of its 
rapidity. 

Variations of Capillary Flow. —A number of factors influence the capillary 
flow. In the winter or in cold weather the flow is retarded in the narrowed 
capillaries, whilst in the summer and in a warm room, the flow is accelerated 
in the dilated capillaries. 

In the vasoneuroses deviations from the normal are recorded. In acro¬ 
cyanosis the flow may be so retarded that stagnation occurs. In hypertonic 
conditions there is a pulsatile flow, and in aortic insufficiency, a true capillary 
pulse can be observed. 2 In arteriosclerosis, there is a slowing and dilatory 
type of current, with marked insufficiency of the circulatory system, char¬ 
acteristic diminution in the rapidity of the flow is observed; even to the extent 
of complete stasis in the dilated venous limbs of the capillaries. Or spon¬ 
taneous reflux from the venous into the arterial limb may take place. Such 
observations must be regarded as of some prognostic import. 

In order to exclude the cardiac factor, Weiss and Dieter 3 did experimental 
work in which the vascular territory examined was suddenly excluded from 
the heart action. Observations thus made were described as applying to a 
closed vascular territory. 

Capillary Circulation in a Closed Vascular Territory. —Weiss and Dieter’s studies were 
carried out as follows. The circulation of an extremity was suddenly brought to a stand- 

1 Weiss, (a) Arch. f. klin. Med. 119, 1-38. (6) Munchen. med. Wchnschr., 1916, 925. 

(c) Munchen. med. Wchnschr., 1917, 609. ( d ) Wien. klin. Wchnschr., 1918, 41. (e) 

Munchen. med. Wchnschr., 1918, 607. (/) Ztschr. f. exper. Path. u. Therap. 19, 390 (1218). 

(g) Ztschr. f. arztl. Fortbild., 16, Nr. 7 (1919). (It) Reichsmedizinalanzeiger, 44, Nr. 1 
(1919). 

2 This is not in accord with the views of other authors. 

3 Weiss & Dieter, Zentralbl. f. Herz. u. Gefasskr., Dec., 1920, p. 295. 


METHODS OF INVESTIGATING CAPILLARY CIRCULATION 65 

still with the use of a pneumatic blood pressure cuff, the previous, coincident and subsequent 
condition of the capillary flow being included in the investigation. In order to avoid over¬ 
filling of the venous territory, a sudden increase of pressure in the cuff was attained by the 
use of a cylinder of compressed oxygen connected with the blood pressure apparatus.. 

After the application of the cuff, selected capillaries are placed into the field, with two 
investigators put in charge. The first observer takes note of the flow in the capillary loop, 
whilst the assistant manipulates the Riva-Rocci (blood pressure) and the oxygen apparatus. 
At the command of the first observer, the cuff is suddenly distended so as to obtain a maxi¬ 
mum pressure (about 200 mm. of mercury). As the mercurial column rises, a stop watch is 
started. . , . 

When the capillary flow ceases, a signal is given to the second observer who times this 
moment. The first observer is not permitted to waver in his watchfulness of the phenom¬ 
ena in the capillary loop, the assistant taking full charge of the time calculations. 

In normal persons at ordinary room temperature, the duration of the capillary current is 
30 seconds. A longer continuation of the flow is caused by equalization in the pressure 
in the arterial and venous systems. At a colder temperature the time of flow is shortened 
by increased tonus and contraction of the vessels. At a higher temperature it is increased 
by dilatation and relaxation of the vessels and there is a back-flow of the blood from the 
venous limbs of the capillaries into the arterial limbs. After plunging the hand momen¬ 
tarily into ice water, the time is shortened at first, but after the passing of the reaction it 
is lengthened. 

In benign nephrosclerosis with marked hypertension there is lengthen¬ 
ing of the time of flow as a result of the marked difference in pressure between 
the arteries and veins. Back flow may take place on account of the 
high tonus. 1 . . . 

Although but few observers have as yet made use of this procedure, it is 
well worthy of an extended trial. Some deductions of value may be expected 
in the early cases of vascular occlusion, when objective manifestations are not 
as yet sufficiently distinct to allow of certain diagnostic conclusions. When¬ 
ever we wish to make inferences regarding the existence of localized vascular 
derangements of function, however, the influences of the general systemic 
circulation with the heart action, must necessarily be excluded. 

(1) The Morphology of the Capillaries—The normal appearance of the 
capillaries at the base of the finger nail is shown in Fig. 29. Here are one 
or two rows of simple loops just proximal to the cuticle, and below them 
manv rows of shorter, comma-shaped vessels are seen. In the first row the 
papillae of the skin are flattened out so that the vessels are viewed running 
horizontally, while in the lower layers, where the papillae are present, only 
the tops of the vertical capillary tufts come to view. In the present state of 
our knowledge we cannot generalize and accept certain capillary pictures as 
pathognomonic of a certain disease (Boas). It appears, however, that 
whenever the vascular system is affected, the capillaries suffer visible altera¬ 
tion, and that this change manifests itself chiefly in an increase in length and 
tortuosity of the vessels. 

This author compares the capillary changes to similar ones in the arteries. 
“Disease of the arteries exhibits itself to the clinician either as a thickening 
of the vessel wall, or as an increase in length and increase in tortuosity 
of the artery. The tortuosity is consequent on the lengthening of the 
vessel, since the distance between the origin and termination of the artery 
remains the same, an increase in length must manifest itself by a greater 
twisting and curving of the vessel.” Anything that tends to increase the 
length of the capillaries, will tend to bring about looping. Two chief factors 
are possible etiologic agents. One is an alteration in the capillary wall 
and the other is a loss of tone due to abnormal nervous control. Thus both 


1 Weiss and Dieter, Loc. cit. 


66 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


organic vascular disease, as well as imperfect nervous control (as in vaso¬ 
motor instability), may bring about structural alterations in the capillaries. 

(2) The Blood Flow in the Capillaries .—There is uniform filling of all of 
the vessels in the microscopic field, and only after a close study will 
the streaming of the blood become apparent. The flow is rapid and con¬ 
stant and never pulsatile, and the blood column in the capillaries is a continu- 


«**<*•• , 

°> S O * ? 

0 t* 


Fig. 29.—Normal capillary picture. (Boas) 

ous one. A vessel may be seen in which the flow is sluggish at times, only 
to quicken in a few moments. No pulsatile flow occurs in the capillaries. 
Cold will retard the flow, while heat will accelerate it. When the capillary 
flow becomes slow, the column of blood no longer has the normal continuous 
and uniform appearance, but is broken into segments separated by colorless 
areas. This may be called a “granular streaming.” It is rarely observed 
in the normal circulation, and when present in many capillaries, indicates 
some disorder of the capillary circulation. The flow of the blood in the capil¬ 
laries may be artifically modified either by inflating a blood pressure cuff that 
has been applied to the arm, or else by inflating the capsule of Danzer and 
Hooker’s microcapillary tonometer. Under such conditions, the capillary 
circulation may be altered at will, and the variations in the flow may 
be studied at leisure. 1 

In acrocyanosis (Fig. 30) the capillaries are longer and more tortuous 
than usual and may present quite a bizarre shape. With this it will be 
observed that during the period in which the hands are cold, there is com¬ 
plete stasis in many of the vessels, and in the others the flow is sluggish and 

1 Boas, Loc. cit. 


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METHODS OF INVESTIGATING CAPILLARY CIRCULATION 


67 


irregular. The blood pressure in these capillaries is very low. Immersion 
of the hand in hot water provokes a remarkable change. The hand becomes 
bright red. Under the microscope we see the blood streaming rapidly 
through the capillaries, and all signs of stasis have disappeared. At the 
same time the capillary blood pressure has risen to a normal figure. 

The following observations were made in cases of thrombo-angiitis 
obliterans by Boas. It was noted that but few capillary loops were visible. 



Fig. 30.—The capillaries of the finger in a case of acrocyanosis. (Boas) 


After rubbing the area of skin under observation with a blunt instrument, 
many anastomosing and branching capillaries came into view. These 
observations lend themselves to the interpretation that many of the capil¬ 
laries were tightly contracted, permitting the passage of no blood until the 
mechanical stimulus brought about their relaxation. 

Spasms of the capillaries have been observed in Raynaud’s disease (Hal- 
pert 1 ). During an attack, although the number of capillaries visible remain 
unchanged, the larger capillaries become fuller, especially their venous loops, 
and their contour changes. In severe attacks the capillary flow ceases; 
but in the larger capillaries the blood is pushed through the vessel in a peris¬ 
taltic-like wave. Pribram and Henius describe a similar peristalsis of the 
capillaries in the stage of ischemia. 

(3) The capillary blood pressure can be estimated with Danzer’s and 
Hooker’s microcapillary tonometer. The part is kept at heart level during 
the test in order to avoid the hydrostatic effect of the column of blood. The 
figures given are 15 and 30 mm. of mercury for normal individuals. Read- 
1 Halpert, Ztschr. f. ges. exper. Med., 11, 125, 1920. 



68 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


ings, however, may vary with the finger examined. According to recent 
observations the variability has been on the average 18 mm. Absolute 
figures cannot be given. It is said that when the readings tend to be above 
30 mm. Hg., the capillary pressure is high; when they are below 15 mm. Hg., 
the pressure is low. 

The Results of the Tests. —Recent observers have studied the capillaries 
in acrocyanosis from the morphologic standpoint, in regard to the character 
of the blood flow, and also as to the capillary pressure. The method of 
Danzer and Hooker is recommended for capillary blood pressure estimations. 
These authors describe a microcapillary tonometer by means of which esti¬ 
mations can be carried out with some accuracy. A practical, convenient 
technic was developed. The principle was introduced, to wit, that the cessa¬ 
tion of the blood flow in the capillaries, rather than the disappear¬ 
ance of the capillaries marks the proper pressure at which the reading should 
be taken. 1 

They found that the normal capillary pressure ranged from 18 to 22 mm. of mercury; 
but that in any individual most of the readings on different capillaries varied from 6 to 7 
mm. of mercury although in many capillaries the difference was greater. They, however, 
discarded the very high and the very low readings and took as the capillary blood pressure 
the average of those which did not exceed this variability. 

Boas 2 in a personal communication reports that he had examined 12 patients who 
exhibited acrocyanosis of various forms from the mildest to the more severe degrees, 
employing the technic of Danzer and Hooker, except that the finger of the patient was not 
scrubbed for fear of introducing a complicating factor. 

Although the cases examined by this author, and some of those who are to be quoted as 
applying these newer procedures for the study of the capillaries are referred to as “acrocya¬ 
nosis,” they may not truly belong to the group we have elsewhere discussed. 3 All that can 
be said is that cyanosis of the peripheral parts was doubtlessly present. 

The capillary blood pressure was found low in every case. He says that the normal 
capillary pressure as determined by this method, varies from 20 to 30 mm. Hg., and that 
another striking feature, is the lack of variability of the capillary pressure. In patients 
with normal or high capillary pressure, the individual readings made on different capillaries 
usually show a variation of about 20 mm. Hg. “The capillary pressure in 10 readings 
registered 2 or 3 mm. Hg., and on 1 capillary only was a reading of 17 mm. obtained. The cold 
hand was then immersed in very hot water, and became bright red in color. The capillary 
pressure taken immediately was from 19 to 20 mm. As the hands slowly cooled and again 
became pale and blue, the readings dropped first to 13 and then to 8.5 mm. It was strik¬ 
ing, too, to observe the change in the blood flow in the capillaries. When the hands were 
cold and blue, the streaming was very sluggish and irregular, but after the hot water bath it 
became very rapid and the capillaries became full.” 

From these observations the author concludes, that when the hands are cold and cya¬ 
notic, the capillary blood pressure is low and the flow sluggish. According to his view this 
cannot be due to a constriction of the venules, but must depend upon a constriction of the 
arterioles or a marked dilatation of the capillaries. It is significant, too, that the capillaries 
become fuller when the hands become warm. If the venules were constricted, the capil¬ 
laries would be engorged during the period of cyanosis. 

Regarding the morphology of the capillaries in acrocyanosis 4 Weiss noted 
that in patients of an asthenic build, who often exhibit acrocyanosis, the capil¬ 
laries are more tortuous than normal, particularly in the venous portion, and 
that the blood stream is slow and may even at times be completely arrested. 
“In the vasoneuroses he saw contractions of the arterial limb of the capil¬ 
laries in ischemia and a dilatation of the venous limb when the hands became 

1 For a critical survey of methods to determine capillary pressure see Friedenthal, 
Ztschr. f. exper. Path. u. Therap., 19, 2, 1917. 

2 Boas, Studies from Montefiore Hospital, 1922. 

3 Chap. XCV (Chronic Acroasphyxia). 

4 Note that the term “acrocyanosis” as used here, is a more general designation for a 
cyanotic condition of the peripheral parts. 


GENERAL CIRCULATION UNDER PATHOLOGICAL CONDITIONS 69 


blue. The appearance of the capillaries, as well as the speed of the blood 
stream, may vary from moment to moment. Warming the hand accelerates 
the blood flow in the capillaries. Mertz 1 found long and tortuous capillaries 
in children with vasomotor instability. Parrisius 2 observed a movement 
which he likened to peristalsis in the venous arm of the capillaries in a patient 
with local asphyxia of the feet. This caused an interruption in the con¬ 
tinuity of the blood column. He also noted changes in the form of the capil¬ 
laries in the vasoneuroses. In a case of Raynaud’s disease Weiss saw very 
wide capillary loops, which exhibited variations in caliber. In a similar case 
Pribram and Henius 3 observed a capillary spasm associated with the 
ischemia. Halpert 4 described in detail the capillary changes in a patient 
with a typical Raynaud’s syndrome. She found increased tortuosity of the 
capillaries, as well as groups of capillaries 3 to 5 times larger than normal. 
The blood flow was slow. During an attack the giant capillaries became 
fuller, especially in their venous portion, and exhibited changes in contour, 
such as projections and strictures. The blood appeared to be pushed through 
the vessel by a peristaltic-like wave. In a severe attack the blood became 
completely stagnant and blue.” 

Leriche and Pollicard point out that in Raynaud’s disease the capillaries 
may become almost invisible as the integument becomes blanched. The 
lateral branches of the capillary loop become filiform, whilst the summit of 
the loop may remain unchanged enclosing the retained blood cells. Only 
slight reduction in the lateral branches may occur in the mild attacks. After 
the crisis is over, dilatation of the whole capillary loop occurs. 

These authors conclude that besides arterial spasm, capillary spasm occurs in Raynaud’s 
disease. The subsequent capillary dilatation may be explained on the theory of the action 
of chemical metabolites (humoral theory) according to which accumulating toxic products 
resulting from poor oxygenation and metabolism produce diminution in the tonus of the 
capillaries. 5 


CHAPTER IX 

GENERAL CIRCULATION UNDER PATHOLOGICAL CONDITIONS 6 

From a study of the function of the peripheral vessels, many of the patho¬ 
logical phenomena observed in the diseases of the vessels of the extremities 
will be better understood. The task of the vessels is to deliver to any organ 
or part of the body the necessary quantity of blood. This necessitates a 
normal functional activity of these channels. The requisite quantity adapts 
itself essentially to the needs of such oxygenation as may enable tissue respira¬ 
tion to go on. The aim is to deliver nutritive substances, and to take away 
products of metabolism. The need for oxygen seems to be the motivating 
factor in the functioning of the vessels. The physiological activity of the 
vessels is of reflex nature. 

1 Mertz, Deutsch. med. Wchnschr., 46, 480, 1920. 

2 Parrisius, Pfliiger’s Arch., 191, 217, 1921. 

3 Pribram and Henius, Berl. klin. Wchnschr., 57 , 67, 1920. 

“Halpert, Zeitschr. f. ges. exper. Med., n, 125, 1920. 

5 Since the above was written further researches have warranted the inclusion of 
additional data summarized in Chap. CVI. 

6 The derangements of the circulation following peripheral nerve lesions are described 
in Chap. XCI. 



70 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Disturbances in the mechanism can arise, firstly, through paralysis of 
the vessel muscle, with consequent dilatation of the vessel and loss of the 
regulatory influences; and secondly, through rigidity of the vascular walls 
of organic nature preventing adaptation of the lumen of the vessel to the 
requirements or diminishing the degree of response. 

Vascular Insufficiency. —When either of the above conditions obtain, we 
may speak of vascular insufficiency. In other words, loss of tonus or increased 
tonus is responsible for impairment of the work of the vessels, and may lead to 
insufficiency of these. Palpation of the pulses gives but a limited notion of 
the tonus, permitting us to differentiate between hard, soft, dicrotic pulse, 
etc. 

A distinction has been made between an active or passive hyperemia of 
organs, or of the skin. The power of adaptation or response of the vessels to 
thermic irritants (cold or warmth) depends upon the intactness of the essen¬ 
tial vasomotor nerve functions. Exercise or muscular exertion with its 
attendant demands on the muscle tissues will normally effect dilatation of 
the afferent arteries, with increased rapidity of blood flow through the parts. 

Where the vasoconstrictor influences fail, the arterial sheath becomes 
relaxed, and the tonus falls. This condition is seen in Addison’s disease, 
where there is a lesion of the adrenals and implication of the chromaffine 
system. In this condition, adrenalin only will act as a stimulant of the, sym¬ 
pathetic system. In the normal blood the adrenalin has a tonic effect on 
the vessels. In Addison’s disease there is diminution of adrenalin production, 
and a decrease in blood pressure that can be artificially and temporarily 
increased through injection of the drug. 

Statements such as these, in which the literature abounds are not quite in consonance 
with the views of others. For it is asserted, of late, 1 that the chromaphile tissues do not 
maintain, nor help maintain the normal tone of the blood vessels or other sympathetically- 
innervated structures. Nor is the medulla of the adrenal body essential to life. 

The condition described as “war edema” is another instance of gen¬ 
eralized insufficiency of the vasomotor system. In this disease the kidneys 
are intact and there is marked salt retention, bradycardia and diminished 
blood pressure: a true example of chronic hypotonia. Furthermore, in acute 
fevers, such as epidemic grippe, a sudden failure or insufficiency of the vessels 
has been noted, particularly as a complication of pneumonia. 

Localized Derangements of Vascular Tone. —Diminution of the vascular 
tonus can be brought about through the action of hot baths; and a compen¬ 
satory vasoconstriction in other territories is said to occur. There is be¬ 
lieved to be a certain antagonism in the bearing of the skin and of the internal 
organs as far as the vessels are concerned. When there is marked muscular 
activity, the vessels of the splanchnic territory are said to contract. Transi¬ 
tory increase in tension of the vessels of such territories has been described as 
giving rise to vascular crises (Pal 2 Hoffman, 3 and Fahr 4 ). 

According to this theory the vessels (abdominal, thoracic, cerebral terri¬ 
tories, or in the extremities) may react by contraction to certain stimuli; 
even Raynaud’s disease and intermittent claudication are regarded by some 
as examples of such effects(?). 

1 Pearlman & Vincent, Endocrinology, 3, 1919, p. 121. 

2 Pal, Gefasskrisen, Leipzig, 1905. 

3 Hoffman, Jahresk. z. arztl. Fortbild., 1919, p. 3-18. 

4 Fahr, Zentralbl. f. Herz. u. Gefasskr., 1918, H. 3, p. 25. 


LOCAL CIRCULATION 


71 


\ ascular insufficiency can also be well studied in arteriosclerosis. This 
disease may affect all of the arteries, or may be localized: arteriosclerosis 
of the aorta, the coronary artery, vessels of the splanchnic territories, 
vessels of the kidney, brain and extremities may be given as examples. 
Therefore, localized disturbances are to be expected in the territories sup¬ 
plied by the affected vessels. The normal regulating mechanism in these 
territories must be more or less in abeyance. 

Peripheral arteriosclerosis can exist with little or no involvement of the 
vessels elsewhere. The evidences of arterial insufficiency are particularly 
manifest in the muscle territories. Because of the intensive demands of the 
working muscles, the arteries cannot allow of adequate supply when certain 
functional disturbances arise. This is particularly the case in the lower 
extremities, where so-called intermittent claudication is the clinical expres¬ 
sion of these disturbances. 

In Raynaud’s disease and erythromelalgia, insufficiency or malfunction 
of the nerve mechanism of the vessels is believed to exist. 


CHAPTER X 

LOCAL CIRCULATION 

A discussion of the pathological local circulation should comprise the 
alterations due to diminished blood supply (local anemia or ischemia) and to 
increased blood content (local hyperemia including rubor and erythromelia). 

LOCAL ANEMIA OR ISCHEMIA 

Causes. —Whenever a given circumscribed part of the body receives less 
than its normal quantity of blood or almost no blood, we speak of local hypemia 
(or ischemia, namely diminished blood content) or of Ideal anemia (failing or 
absent blood content). A part is practically never completely depleted 
since some blood always remains in the vessels. Custom, however, permits 
us to extend the appellation anemia even to those states in which the blood 
depletion is incomplete. Some of the continental physiologists have been 
wont to make use of the term local hypemia , to more accurately designate a 
state of diminished local circulation. 

The author has for years employed the word ischemia to designate that 
condition in which certain obstacles to, or checks upon the normal circulation 
manifest themselves in a part. One may even in the normal, produce slight 
local anemia (or relative anemia) through the mere elevation of a part, by 
virtue of which the venous return is enhanced and the delivery of blood 
made more difficult. 

There are a large number of other coefficients that influence the 
production of ischemia. Amongst these may be mentioned the following: 
the mechanical factors of obstructive arterial disease, the effect of drugs 
(adrenalin), thermal and mechanical forces as well as neurogenic, and even 
psychic influences. The lumen of an artery may be reduced, or wholly 
abolished through thrombosis or embolism, or from alterations in the struc- 


72 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


ture resulting from disease processes (luetic endarteritis, atherosclerosis, 
thrombo-angiitis, etc.). Local ischemia may also be the sequel of the mere 
contraction of arteries of supply, or even of capillaries. Such results are 
attributable to forces acting directly or indirectly through the nervous 
system. Adrenalin may act directly as a vasoconstrictor, as also, ergotoxin , 
the alkaloid that is responsible for the condition of ergotism. Cold also 
contracts the vessels. A varying predisposition to thermic influences finds 
an illustration in the extreme susceptibility exhibited by the cases of “dead 
fingers” or doigt mort due to moderate degrees of cold. The fingers of such 
individuals may suddenly become pale, cold and even livid immediately 
upon immersion in cold water. Here there is an illustration of vasocon¬ 
striction through reflex nerve paths. Here neurotic phenomena may even 
cause the skin vessels of one arm to contract when only the other arm is 
exposed to cold. 

In addition to these factors, there are also those motivating agencies that 
evoke arterial spasm in the presence of a spasmophilic tendency. These 
evince their most exquisite manifestations in Raynaud’s disease. 

As for the newer theories on the physiology and pathology of the vege¬ 
tative system, we refer to Chaps. V and VI, in which both the role of the 
calcium salts, the endocrines and the vegetative nervous apparatus have 
received due consideration. 

Local anemia or ischemia may arise through increase of the outflow 
without corresponding increase of the inflow of blood; through mechanical 
displacement (compression) and through diminution of arterial influx up to 
complete cessation of flow (complete ischemia). 

We are interested here not so much with the first two of these. The last 
will be described in further detail, since most of the maladies leading to cir¬ 
culatory derangements of the extremities belong to this type. 

Diminished Arterial Influx. —A number of causes for this type of ischemia 
must be considered: (i) deficient filling of avascular territory; and (2) defec¬ 
tive filling by reason of primary diminution of the size of the afferent vascular 
lumina. 

1. A vascular territory may be poorly supplied (a) by reason of abnor¬ 
mality of heart action; ( b ) because of depletion due to the deflection of blood 
into other territories or organs; and ( c ), defective vascular fulness in non¬ 
functionating paralytic parts. 

We need not dwell upon these well-known causes, since the student will 
have received adequate knowledge thereof in his reading along other lines. 
It may be well to confine the discussion, therefore, to the second type where 
the afferent vessels are narrowed either mechanically or functionally. 

2. Mechanical Diminution of the Patency of the Arteries. —The consequences 
of mechanical closure of a vessel through ligation, compression, embolism, 
thrombosis or advanced mural changes depend upon the time during which 
the occlusive process is elaborated and more particularly upon the presence 
or absence of collateral connections with other arteries. The immediate 
effects upon the territories supplied, the clinical manifestations and the 
responses that are evidences of Nature’s compensatory processes, are fully 
described elsewhere. 

Neuro-irritative or spastic anemia or ischemia may be produced by local 
contraction of small vessels. Functional contraction of arteries may take 
place through direct action such as cold, through chemical influences, or 
through the nervous system. These various types will also be given due 
consideration. 


LOCAL CIRCULATION 


73 


The Consequences of Local Ischemia. —The striking visible evidence of 
impaired and diminished circulation of a part is the change in color or pallor 
(blanching). Careful observation may then demonstrate also a certain 
degree of diminution in volume of the part. The latter, however, is due in 
part also to the reduction of quantity of tissue fluids other than the blood. 
When ischemia continues over a sufficient period, the part becomes cooler 
because of the limitation of amount of blood delivered and altered chemical 
activity. Functional derangement of the cells, too, results. In short, 
alterations in color , volume, temperature and function appear, and they vary 
according to the degree of circulatory deficiency, its rapidity of onset, its 
duration, the possibilities of collateral compensation in the affected terri¬ 
tory and the susceptibility of the part or organ involved. Naturally the 
amount of circulatory impairment depends on the degree of obturation of 
the supplying vessel, and the number of vessels implicated. 

So also, the advent of the obstructive factor will, to a degree, determine 
the issue; a sudden embolic closure being more to be feared than slower 
obturating processes. 

The duration of interference, too, is important in that temporary forms of 
pressure are relatively insignificant in their effects as compared with lesions 
due to embolism, thrombosis, or disease of the vessel walls. 

The collateral blood supply may be a determining factor. Normally, 
certain preexisting channels are present, which in the face of obstructing 
agencies, act as devious surrogates in which an abnormally high blood pres¬ 
sure is produced. 


HYPEREMIA 

Another result of circulatory derangement is the condition of arterial 
hyperemia. Active hyperemia has been employed to characterize the circu¬ 
latory condition in an organ in which the blood flow is one of its functions. 
There may, too, occur hyperemias of paralytic nature with lesions of vessel 
nerves. 

For the establishment of hyperemia, dilatation of arteries is a sine qua non. 
In the normal, such change in the lumina takes place by virtue of nerve 
action, either through stimulation of the vasodilators or diminution in the 
tonus of the vasoconstrictors, or both. The facial blush is a common example 
of arterial hyperemia. In particularly susceptible individuals the normal 
relationship between blushing and the motivating factors is disturbed. So, in 
addition to the usual exciting moment of shame, minimal irritants such as 
warmth may suffice to bring it about. 

In conditions of neuroparalytic hyperemia with paralysis of the vasocon¬ 
strictors, (except after section of the cervical sympathetic), it may be diffi¬ 
cult to establish the neurogenic character of arterial hyperemia. Although 
we know from experimental work that excitation of various centripetal nerves 
may cause arterial hyperemia, it is very hard to recognize the provocative 
factors in the human. Investigations have shown that the intensity of the 
irritant may determine whether constricting or dilating effects are obtained. 
Stimulation of sensory nerves has been followed by local vasodilatation and 
constriction in more remote territories. 

Increase of the surrounding temperature usually causes dilatation of the 
cutaneous vessels (a reflex effect). 


74 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Many erythemata are of nervous origin, such as symmetrical hypere- 
mic spots (taches cerebrales). In diseases of the spinal ganglia (with 
herpes), arterial hyperemia may follow excitation of vasodilators. The 
vasodilator paths are supposed by some to be identical with the centripetal 
nerves which, therefore, would functionate in an antidromic sense. 

As for the substances that are able to exert a direct dilating effect on the 
vessels, it has not as yet been established whether their action is through 
peripheral endorgans of the vasodilators or by virtue of a paralytic action on 
the vessel musculature. These substances, however, show a selective action 
in that they may cause dilatation of some, constriction of other territories. 

The postanemic hyperemia following the cessation of compressing forces 
(tourniquets, Esmarch bandages,) is an example of arterial hyperemia. Its 
clinical analogy can be produced when we elevate an extremity in which 
arterial occlusion is present, wait for ischemia to develop and subsequently 
allow the limb to hang down. A marked reactionary or induced rubor 
(erythromelia 1 ) is a characteristic phenomenon. Its intensity is greater 
than the chronic hyperemia which may or may not already be present in 
obstructive arterial disease. 

Some physiologists attribute the establishment of postanemic hyper¬ 
emia to reflex nerve action. It is known that such hyperemia may follow 
section of a nerve. But this does not preclude the local influence of, neuro¬ 
genic impulses; for both anemia and sudden return flow of blood into an area 
previously excluded from the circulation may bring about local excitation of 
nerves. As examples of such may be cited the fibrillary contractions of 
muscles when blood reenters anemic parts. These occur even after section 
of the motor nerve, but are put in abeyance after curarization. From this it 
can be concluded that irritation of the motor nerve endings in the muscles is 
responsible for the phenomenon. 

Vasoconstriction and even vasodilatation are usual and common sequences 
of obstructive anemia or ischemia. Both of these may be of neurogenic 
origin. Clinically, analogies will be brought to the reader’s attention in 
the discussion of the vasomotor manifestations accompanying hydrostatic 
(mechanical) phenomena in thrombo-angiitis obliterans. Here we may 
merely mention that a chronic or more or less permanent hyperemia is one 
of the characteristic manifestations of the disease. Its origin is probably 
in part hydrostatic and mechanical, and in part neurogenic. After elevation 
of the limb in this affection, ischemia is manifested by the blanching of the 
part; and if the limb be subsequently allowed to hang down, an excessive 
amount of rubor, quite out of proportion to the degree usually present, is 
evoked. This corresponds to the above described postanemic hyperemia 
(induced, reactionary rubor). 

Singular and noteworthy examples of neurotic vasomotor constriction 
can be frequently demonstrated. It was pointed out, above, that both 
temporary vasoconstriction and more or less prolonged vasodilatation are 
the neurotic effects of ischemia of the parts. A clinical example may often 
be observed in thrombo-angiitis obliterans. For if a limb be made to 
blanch for an adequate period of time in this disease of obstructive vascular 
nature, and the part be then gradually brought down towards the horizontal 
or below this level, a gradual blush (hyperemia) will be observed to travel 
from the periphery in a central direction. Strange to say, however, the 
pallor may persist in the horizontal position for sometime, even though it 
had been previously proven that a fair degree of color was the rule in this 

3 A term employed by the author and elsewhere described in extenso (Chap. XLVI). 


LOCAL CIRCULATION 


75 


posture. Or islands of color may be of prolonged duration. These two phen¬ 
omena, although presumably in part of mechanical or hydrostatic nature, 
can be more readily explained on the assumption that the neurogenic vaso¬ 
constriction induced by the anemia is unduly sustained , and the reactive 
vasodilatation (rubor hyperemia) correspondingly delayed. 

Venous Hyperemia. —This is essentially the opposite of local ischemia for, 
whilst the former arises through impediments to the inflow of the blood, the 
latter is due to defective outflow. As a rule, mechanical causes are at work 
so that we speak of mechanical or passive venous hyperemia. The large 
number of collaterals prevents any appreciable interference with the outflow 
when but one or a few channels are obstructed, except when one of the larger 
trunks is involved. 

Although it is usually believed that the veins themselves play a passive 
role, the possibility of a functional participation of these channels has been 
suggested by the results of experimentation. 

Cardiac insufficiency may cause venous stasis, or when with increased 
intrapulmonary tension, the outflow through the veins is impeded. In 
the extremities the insufficiency of the valves of the veins adds to the diffi¬ 
culties of the venous transmission of blood, and in these circumstances, the 
effects of gravity are felt. Any muscular contraction or cramp may be a 
further impediment. 

The absence of venous tone should also be mentioned as another such 
factor. External (particularly constricting) pressure, thrombosis and endo- 
phlebitis have an obstructive action. 

The consequences of venous hyperemia in a part are: dilatation of visible 
veins, cyanosis, increased volume of the affected region, and diminished 
temperature. The cyanosis is not essentially due to the enlargement and 
engorgement of the visible channels, but rather to the alteration in the color 
of the blood. This is a sequence of the diminished arterialization and the 
greater carbon dioxide content that the retarded flow brings about. In 
contrast to the effect of arterial hyperemia, reduced warmth is often char¬ 
acteristic of stasis. 

Venous blood, according to Krogh, never induces any local contraction of 
capillaries, but often a pronounced dilator action; the latter may, however, 
be counterbalanced by strong constrictor stimuli that exert their action 
directly or through sympathetic nerve fibers on the capillaries’ contractile cells. 

Acrocyanosis. —A dusky discoloration (often spoken of as asphyxia or 
cyanosis) of the fingers, hands and the feet, may occur in a number of differ¬ 
ent affections. In some of these the general circulatory conditions are at 
fault, in others the constitution of the blood; and, in still others there are 
transitory, sometimes fugitive periods of vasomotor instability. 

The Asphyxia of Irritable Hearts. —Abnormal changes of color, such as 
lividity or pallor, are frequently noted in the extremities of patients suffering 
from irritable heart (Briscoe). The usual agent inciting color changes is 
cold. Washing the hands in cold water, or a sudden change of room tem¬ 
perature, conditions that would ordinarily not affect normal individuals, seem 
to call forth the peripheral asphyxia. 

There are cases too, in which the hands are said to be livid, cold and numb 
at all times, the discoloration involving the fingers, the hands, and even the 
wrists, with often a bluish tinge over the forearm. The compression or 
expression test 1 produces a dead white patch that evidences the sluggish- 

1 Described on page 163, as a rough index of circulatory activity; but it is dependent 
on vasomotor influences. 


76 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

ness of the circulation, for the color is but slowly regained. The color of 
the blood, too, when allowed to ooze out through a pin prick, is very dark, 
so that we have here three essential features suggestive of retarded capillary 
circulation and venous stasis; namely, coldness, darkness of the blood, and 
sluggish return. The mucous membranes are not cyanotic. 

From experiments on capillary pressure in reflex response to cold, 
Briscoe 1 concludes that the immediate reaction to cold is a transient fall in 
capillary pressure probably due to a constriction of the arterioles. For this 
would diminish the supply of the blood to the capillaries and reduce the pres¬ 
sure. But a simultaneous contraction of the venules would compensate and 
bring the capillary pressure up to normal again, in spite of the diminished 
flow through the extremities. That reaction to cold may be of remote nature 
has already been mentioned. When one hand is placed in cold water, it has 
been demonstrated that the flow of blood through the other hand is cut down 
to nearly one-half (Stewart 2 and Hewlett 3 ). An increase in irritability of 
the vasomotor system, as is known to exist in Raynaud’s disease, was also 
brought to light through the studies of Stewart, when in his experiment of 
immersion of one hand in cold water in a case of Raynaud s disease, the flow 
in the other hand was instantly reduced. 

In acroasphyxia attending cardiac irritability, the capillary pressure rises 
above the normal, while in controls it does not quite return to normal. 
From this it has been concluded that there is a vascular spasm distal to the 
capillaries, namely, in the venules. With sufficiently long continued spasm 
the velocity of the blood stream is diminished and the blood becomes venous. 

The pinkish areas in cases of blue hands have been explained on the theory 
that the mechanical alterations in the blood, due to increased carbon dioxide 
and other metabolic products may bring about dilatation of arterial capil- 
laries by direct chemical action. 4 


CHAPTER XI 

FUNCTIONAL DISTURBANCES OF PERIPHERAL CIRCULATION 

These may be divided according to their main functions into 
derangements due to altered or inadequate blood circulation and into 
abnormalities of the fluid exchange through the capillary walls. These two 
are in intimate relationship; indeed, the latter being in a measure dependent 
on the former. 

i. Derangement of the Capillary Flow— Variations in rapidity of capil¬ 
lary flow are observable in different territories. A distinction can be made 
between the capillaries, the precapillary arteries and postcapillary veins. 

Increased blood pressure can intensify the flow in the capillaries when 
these are not narrowed. In hypertonic conditions (nephrosclerosis) the 
capillary flow has been found accelerated; so also in aortic insufficiency. 
Where the capillaries are narrow as in marked arteriosclerosis, retardation 
occurs. A slow flow has been noted in acrocyanosis, in Raynaud’s disease, 5 

1 Briscoe, Heart, V. 7, 4, 1920, p. 43. 

2 Stewart, Heart, 1911-12, III, 76. 

3 Hewlett, Arch. Int. Med., 1911, VIII, 591. 

^ See Chaps. XI, XIII, LXXXVII. 

5 For the latest views on Capillary Microscopy in this disease see Chaps. C\ I et seq. 



FUNCTIONAL DISTURBANCES OF PERIPHERAL CIRCULATION 77 


erythromelalgia, scleroderma, and the passive hyperemias of cardiac or 
vascular origin. In general we may say that increased pressure in an artery 
of supply due to narrowing of the latter, causes retardation of the capillary 
stream. 

The changes in capillary flow result in corresponding alterations in capil¬ 
lary blood pressure. This endocapillary pressure is increased both in active 
as well as in passive hyperemia, whilst it is diminished in ischemic conditions. 
With too great a diminution of endocapillary tension the nutrition of the 
part must suffer; some injury, too, ensues upon too intensive an increase 
of pressure. 

As a consequence of a rise in endocapillary tension, diapedesis of the red 
blood cells is a common occurrence, particularly with passive, but also with 
active hyperemia. The character of the capillary wall, however, also plays a 
role in this filtration. A predisposition or hyperpermeability may be 
acquired by the capillaries through the induction of artificial ischemia (post- 
anemic diapedesis). A predisposing factor, therefore, is artificial ischemia, 
which may be observed after the use of an Esmarch bandage. Old people 
are especially susceptible. Diseases, too, that alter the constitution of the 
vessels (scarlet, grippe, etc.) may also increase the susceptibility to diapedesis. 

These observations are of some clinical importance in that they teach 
the lesson that the production of too intensive ischemia through whatever 
means should be avoided whenever marked obstructive disease of the arteries 
of an extremity is at hand. The application of an Esmarch or Martin 
bandage for purposes of making functional tests is not without danger, for 
irrespective of the perils of thrombotic sequels, the extravasation of red blood 
cells may predispose to local necroses and gangrene. So, too, the application 
of the author’s postural treatment 1 for enhancing the circulation and nutri¬ 
tion of the part, must be so carried out that the period of induced blanching 
is minimal. 

Through the same action a migration of leucocytes, too, may take place 
(leucodiapedesis). Because of the spontaneous activity of these cells, we 
usually substitute the word emigration for diapedesis. With retardation of 
flow the white cells approach and are heaped against the vessel wall. Their 
transmigration goes on, both through filtration and their own motility. 

Arterial spasm , when it involves larger vessels as in Traumatic Angio¬ 
spasm, gives clinical pictures quite different from those following con¬ 
traction of the arterioles. When the latter contract strongly, the blood 
still seeks the veins through the force of the vis a tergo, the capillaries becom¬ 
ing emptied. With this the part blanches and its volume may become 
lessened. As the veins fill and the pressure therein overbalances that in 
the capillaries, the part may become cyanotic, and even regurgitation of 
venous blood may take place. This condition becomes accentuated when 
the affected part is in a dependent position. 

If we test for return of color after digital expression (compression test) 
in asphyctic skin in which the arterioles are constricted and the capillary 
circulation poor or nil, the reappearance of cyanotic color must not be 
mistaken for evidence of circulation, for it is but the venous blood com¬ 
ing into view. 

Spasm of venules is said to be possible, but without arteriolar contraction 
the immediate blanching is absent. Lividity is produced through stagna¬ 
tion of the blood in the capillaries. A generalized spasm of arterioles and 

1 See treatment of arteriosclerotic vascular disease and thrombo-angiitis. 


78 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


venules is said to occur, and this is followed by ischemia of the part (anemia). 
Associated is a reduction in volume of the part. 

2. Disturbances Due to Impaired Exchange of Fluids. As far as we 
know, the capillary walls have partial permeability, not allowing all substances 
to pass equally well from both sides. The chemical bodies of the absorption 
stream (from the blood into the tissues) are also different from those of the 
excretion or outflowing stream (from the tissues into the blood). These 
functional elective powers disappear as the tissues lose their vitality. For all 
the phenomena are not explicable on the basis of filtration, diffusion and osmo¬ 
sis, but a capillary secretory activity may play a role. The locality of the 
interchange is probably the intercellular spaces. Alterations in the fluid 
stream may be of quantitative and qualitative nature. 

The changes in capillary pressure also modify the fluid exchange. If we 
accept the theory that diapedesis may be a sequence of the above, we must 
also be ready to believe that analogous alterations in the fluid waves may 
ensue. Indeed, in the occurrence of postanemic edema, we have an example. 
After artificial hyperemia, an intensified lymph current has been noted as 
an accompaniment of the increased absorption stream. A diminished capil¬ 
lary pressure can evoke an increase in the excretory or outflowing stream. 

An excess of capillary pressure may cause fluids to percolate outwards 
from these channels; and the increased intercapillary tension may follow 
local arteriolar dilatation, venular contraction or venous obstruction, edema 
resulting from obstruction to venous flow. It is not certain as to what role 
forces other than mere filtration, play in this abnormal fluid exchange. 
The theories set forth are that the sluggishness of the capillary flow increases 
the permeability of the capillary walls; or, that certain alterations in the 
metabolism of the tissues outside of the capillaries make for increased fluid 
imbibition from the blood. 

For an understanding of some of the trophedemas and conditions of neuro¬ 
trophic nature that are dependent on deranged capillary function, it may be 
well to point out that although intracapillary pressure is often responsible for 
pathologic phenomena in the tissue currents, the condition of the capillaries 
themselves may be the more important. So we have on the one hand, the 
nutritive disturbances of the capillaries due to anemia and passive hyperemia; 
but, on the other hand, the alterations that certain substances may produce. 
Many bodies may increase the activity of the absorption stream. Some are 
specifically vessel poisons such as the toxin of diphtheria, tuberculin, pneu¬ 
mococcus serum, etc. But even for the action of these substances a certain 
predisposition or idiosyncrasy is necessary. (This is seen in the abnormal 
susceptibility of certain individuals to strawberries and shell food.) 

Some authors believe that the tissue stream may be modified through nerve 
influences. These may be manifested in the production of a neurotic hypere¬ 
mia as well as in an altered permeability of the capillaries. The urticaria 
following mechanical irritation of the skin is an evidence in favor of such 
a function. Whether a preceding or coexisting reflexly evoked hypere¬ 
mia is responsible wholly or in part, is still a mooted question. In the 
evanescent edemas without hyperemia, a direct neurogenic basis is probably 
present. 

The administration of calcium chloride tends to reduce the permeability of the capillaries 
and is therefore of value in circumscribed edemas. Increased density of the cellular mem¬ 
brane through increase of calcium content as well as the opposite effect on intensified 
permeability in the deficiency of calcium salts, are well known biochemical and physiological 
observations. 


FUNCTIONAL DISTURBANCES OF PERIPHERAL CIRCULATION 


79 


To digress for a moment, it may be well to call attention to the theories 
of some of the more recent investigators on the vegetative system regarding 
the role of the calcium salts in spasmophilic tendency. According to these, 
defective calcium metabolism with diminution of this salt, may be an impor¬ 
tant factor in the production of hyperirritability of the vasoconstrictor 
centers. 

Functional Derangement of the Lymphatic System.—Although it is 
known that the intercellular spaces communicate with the lymphatics, it is 
still doubtful as to whether they are separated by a thin membrane or not. 
Tissue juices or fluids must not be confused with lymph. All cells are not in 
direct communication with the lymphatics through the tissue fluids, since 
some cells are directly apposed upon the blood capillaries. 

Here, too, quantitative and qualitative changes in function occur. 
Abnormal acceleration or retardation of the lymphatic flow represents the 
former. These may be the result of variations in the production of lymph 
and in its outward flow. 

Mechanical factors, such as pressure, tumor growth, collections of fluid and thrombosis 
may diminish the outflow of lymph. Diseases of the lymphatics and lymph nodes may 
interfere with the lymph flow. When there is increased pressure in the venous system, the 
discharge of lymph into the veins may be impaired. 

Cessation or diminution of lymph flow may set in when the production of lymph is 
correspondingly defective as in arterial ischemia. There are a number of substances that 
increase the lymph flow. Amongst these are hypertonic salt and sugar solutions injected 
into the veins. 

Disturbances of the Lymphatic Stream of Capillary Origin. —Since derangements of flow 
in the capillaries are transferred to the lymph stream, accumulations of fluid in certain 
parts of the body may result. Collections in the tissue spaces are known as edema. 

When a large venous trunk of an extremity is ligated in an animal, there usually follows 
an increased lymph flow without any edema. If we simultaneously interfere with the 
lymphatic flow, or if the blood be hydremic and the vasoconstrictors paralyzed, then edema 
may ensue. In general venous stasis, however, edema appears since by reason of the 
increased venous pressure the lymphatic outflow from the thoracic duct into the subclavian 
vein is impeded. 

Edema usually follows derangement of the capillary walls. It can, however, result 
from alterations in the cells by virtue of which these give off larger amounts of fluid. As 
corollaries, we may mention that transudates seem to indicate an origin through capillary 
lesion, whilst the edemas, because of their salt content, may be more correctly explained on 
the basis of disturbances in the cell function. 

Local fugitive edemas (edema fugax) warrant the supposition that both a local predisposi¬ 
tion of the capillaries as well as neurogenic factors or blood composition, may be at fault. 

Inflammatory edema has several causes including lesions of the capillaries and tissues. 

Disturbances in Continuity of the Vessel Constituents .—Pathologists 
(Hering) speak of solution of continuity in respect to the cells of a vessel 
and a more gross variety in which the cells themselves are broken up. Whilst 
the latter may occur in any vessel, the former applies only to the capillaries 
in which varying degrees of separation of the cells from each other may 
take place. Solutions of continuity may be produced by a large number 
of causes. Mechanical or external agencies, increased pressure from within, 
degenerative processes (atherosclerosis, arrosion) infection with suppura¬ 
tion and necrosis, neoplasms and ferment action—all these are amongst the 
agencies observable. 

In vicarious menstruation, hemorrhages have been attributed to the action of the 
internal secretion of the ovaries as also to neurogenic factors. 

Diapedesis (or the escape of the red blood cells through separated endothelial elements) 
may be altogether due to increased endocapillary pressure into a certain predisposition of 
the vessels themselves. The hyperemias are the exerting moments. In the anemias, the 
factor of susceptibility may be extraordinarily prominent (so also in hemophilias, purpura, 


80 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

etc.). Various poisons alter the fragility of the vessels. We can gain a rough clinical idea 
of the degree of individual susceptibility to diapedesis by comparing the tendency to hemor¬ 
rhages after artificial stasis over a given period with the normal. The usual disposition 
has been characterized as the “endothelial symptom.” 

THE SUPERFICIAL CIRCULATION IN OBSTRUCTIVE VASCULAR DISEASES 

If we were to enumerate the agents through which objectively visible 
alterations in the superficial circulation are modified, we would include: 

(1) The diminished force of the stream (vis a tergo). 

(2) The hydrostatic and gravity forces. 

(3) The changes in the vasomotor mechanism. 

(4) The local forces, that directly influence the autonomic capillary 
activities. 

These all should be taken into account in explanation of the phenomena 
of asphyxia 1 and rubor, 2 so often characteristic signs of the obstructive arterial 
diseases of the extremities. 

1. The Diminished Circulation— To go into a detailed discussion of the 
altered dynamics that are entailed through the exclusion of existing and 
important vascular channels, would be a work of supererogation, For, on 
the one hand, the thesis requires neither emphasis nor explanation for com¬ 
prehension; and on the other hand, an exact measure of the diminution of 
volume and celerity of the blood stream is beyond the pale of our applied 
physiological and clinical methods. We must be content, then, to assume 
the existence of impaired flow, for, we have no accurate means of estimat¬ 
ing the degree of circulatory impoverishment in a given case, beyond that 
knowledge which the rough clinical methods to be described may furnish 
us. 3 Certain it is, that a sufficient reduction of this flow is often obvious in 
those significant pallid feet and legs that are cold and blanched even in the 
horizontal position. That a reduction in the fullness, or even a collapse of 
arterioles and capillaries of peripheral skin and subcutaneous vessels must 
obtain through this mechanical cause alone, may be accepted without hesita¬ 
tion. We have elsewhere called attention to the vasoconstriction occurring 
in arterioles and capillaries as a secondary response. 

2. The Forces of Hydrostatic Nature and the Role of Gravity may require 
but passing mention, since their more detailed workings and manifestations 
will receive attention in other chapters. Through the unnatural imbalance 
between the strength of the pumping mechanism and the increased local 
resistance through the exclusion of larger avenues, and the prominence of 
devious and smaller pathways, conditions are given for an enhancement of 
the effects of gravity and hydrostatic forces. Indeed, the latter are influen¬ 
tial, inversely with the patency of the natural vascular lumina; or they 
modify the objective circulatory phenomena more and more , the greater the 
obturation in the affected vascular territory. 

Whereas the normal limb when elevated above the horizontal, presents 
a pinkish integument even over the most peripheral parts, gravity and hydro¬ 
static pressure may make for complete blanching when larger vessels are 
occluded. And so, the position of the part must be taken into due consider- 

1 Vide, Chap. XLVII, Cyanosis in Thrombo-angiitis. 

2 Vide, Chap. XLVI, Erythromelia. 

3 Except perhaps the method of Stewart (Chap. VI) which has not been extensively 
used. 


FUNCTIONAL DISTURBANCES OF PERIPHERAL CIRCULATION 81 


ation when the fullness of arterioles, capillaries or venules is being investi¬ 
gated or discussed. Whilst elevation may deplete the venules (when the 
veins are adequate for return), depression may make for stasis and asphyxia 
when the propulsive forces are inadequate to force the blood through 
arterioles, capillaries and venules with sufficient celerity. 

3. The Changes in the Vasomotor Mechanism. —Many of the basic 
facts that physiologic researches have brought to light have already been 
summarized in the chapter on anatomy and physiology of the vasomotor 
paths. Here we wish to allude merely to those special circumstances in 
local disease that bring about alterations in the normal mechanism. Such 
occur both in the neurogenic and organic obstructive vascular affections. 
Concerning the former, a more detailed discussion will be relegated to the 
chapters that are concerned with the special classes of vasomotor neurosis. 
The deviations of nerve function in the latter, however, may properly be 
referred to here. 

Nerve malfunction may result from the following causes. 

t. Organic intrinsic , lesions of the vessels and perivascular tissues impli¬ 
cating the terminal nerve distribution. 

2. Perivascular inflammatory and secondary fibrotic processes (thrombo¬ 
angiitis obliterans) influencing the adjacent nerves. 

3. Reflex alterations. 

4. Exhaustive states. 

5. Altered local metabolism and abnormal chemical products in the 
tissues. 

In thrombo-angiitis obliterans the perivascular fibrosis and the inflamma¬ 
tory products of the acute stage may exert an influence on the surrounding 
sensory and motor nerves. Through the former, both pain impulses and 
reflexes with vasomotor responses may travel. That pain alone may evoke 
neurovascular phenomena has been elsewhere mentioned. 

We need only emphasize here the great importance of reflexes on the 
vasomotor functions, for these have been already described. In addition 
to the multitude of impulses that are constantly received from within and 
throughout the body, local changes, metabolic, nutritional and patho¬ 
logic (especially trophic ulcers, etc.) as also external causes (thermal and 
mechanical) may play a role in engendering abnormalities of vasomotor 
function. 

4. Exhaustion. —To what extent an exhaustion of the vasomotor impulses 
of constrictor type can be produced through overactivity, cannot be 
accurately determined. That a recoil into a paralytic state or a passive 
vasodilatation is possible after continued angiospasm, cannot be denied. 
Investigators have shown that certain chemicals may initiate a condition of 
constriction that yields to a palsy with chronic dilatation. So, too, may 
nervous mechanism finally fail, be it through continued and over-excitability 
or be it through reflexes evoked through intense and constant pain. 

5. Chemical Action. —If we base our conclusions upon the data furnished 
by physiologists regarding the effects of chemical alterations in the tissues on 
arterioles and capillaries, and the observations of clinicians, we must assume 
that an abnormal vasomotor mechanism can be induced when pathological 
nutritional conditions obtain. In this way a reversal of a normal vaso¬ 
dilating response into an abnormal vasoconstricting reaction may occur when¬ 
ever an unusual stress (exercise) develops an inordinate amount of poisonous 
constituents in poorly nourished tissues. It has been assumed that the symp- 


82 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

toms of intermittent claudication (page 156) may be brought about in 
this way. 

In arteriosclerosis and thrombo-angiitis obliterans, where circulation is inadequate, 
exercise produces an accumulation of CO2 and lactic acid and a deficiency of O. These 
chemicals are believed to be able to cause a reversal of the vasodilating into vasoconstricting 
reflexes. The cramp-like pains that succeed, have been interpreted as the subjective 
manifestations of this altered physiology. 1 According to Hopkins the normal cycle of 
events in muscular activity consists of two phases separated in time: the first anaerobic 
during which lactic acid is formed; the second aerobic during which it is removed. Only 
with conditions of inadequate oxygenation will this acid accumulate. Perhaps it is this 
chemical that calls forth the reflex. 


CHAPTER XII 

COLLATERAL CIRCULATION 

By the term collateral hyperemia we may designate that arterial flow which 
occurs in the territory adjoining one whose main artery has become occluded. 
The origin of such hyperemia depends upon the nature of the arterial distribu¬ 
tion. Whenever adequate arterial anastomoses are present, as in the case of 
the arteries of the hand or the foot, obturation of one large trunk is imme¬ 
diately followed by deflection of the current into other adequate paths. If 
the arterial connections, however, are insufficient, an anemic focus surrounded 
by a peripheral zone of collateral hyperemia develops. 

The term collateral hyperemia has also been defined as that increased influx of blood 
which may occur into one of a pair of important sister organs, such as the kidneys, when 
the artery of one is occluded or the organ itself has been removed. Certain conclusions 
concerning the physiologic hyperemia occurring in such organs may be extended to the 
peripheral vascular system. Increased blood pressure consequent upon the occlusion of 
a large vessel leading to such an organ would not account for the vicarious hypertrophy of 
the remaining organ; and a reflex irritation of vasodilator nerves has been suggested as a 
more plausible explanation. 2 

Another similar manifestation is the secondary or postanemic hyperemia 
that occurs after transitory arrest of the circulation in an extremity. 

Collateral hyperemia is the prelude to, or preliminary stage of an elabor¬ 
ation of a new collateral arterial circulation after occlusion of an important 
arterial trunk. Its development takes considerable time. Whenever a 
large artery is ligated, collateral flow occurs in reverse direction and usually 
with great rapidity. The development of such a current is proportionate to 
the dilatability of the arteries. In the development of collateral circulation, 
either small arterial anastomoses participate or new ones must be formed. 
As a rule, the anastomosis formation is well marked in a few days. 

In collateral circulation, as well as in that of collateral hyperemia, the 
mechanical factor of increased pressure does not sufficiently explain its origin. 
Continuous dilatation of the arteries presupposes diminution of the tonus to 
nerve influence; and we would suppose an increased tonus after increased 
pressure. The genesis of collateral hyperemia after closure of a large arterial 
trunk, therefore, must be regarded rather in the light of a product of altered 
innervation, possibly of irritation of the vasodilators. Pari passu with the 
dilatation of the small vessels, increased growth takes place, so that large 
thick walled vessels may result from small thin ones. 

1 Hopkins, Harvey Lectures, 1920-1921, p. 210. 

2 See Chapter XLVI on Erythromelia and the explanation of rubor. 



COLLATERAL CIRCULATION 


83 


The collateral avenues are preexisting channels whose total capacity bears 
a relationship to their size (caliber), number, patency and dilatability. Any¬ 
thing which interferes with the accommodative enlargement of these, such as 
sclerosis and congenital hypoplasia, may correspondingly limit their func¬ 
tional value under special stress. The local increase of pressure above the 
point of arterial obstruction is important in the development of the collaterals. 
Its degree is proportionate to the size of the closed vessel, and also influenced 
by the general blood pressure. How delicate the mechanism causing circu¬ 
latory disturbances is, may be concluded from the observation that hyper¬ 
tension may be produced also through reflex causes as well as mechanical. 
It is even believed that the chemical alterations in the anemic territory may 
bring about a rise in tension. So also, dilatation of the collaterals may be 
evoked by reflex as well as mechanical forces. Since the general pressure 
depends on the heart action, the development of collaterals, too, will be 
similarly modified. Weeks and months may be required before the ultimate 
collateral circulation has been formed. 

Bolognesi 1 performed experiments to determine the effect of ligating the external iliac 
artery in dogs. The ligation was done with a double catgut ligature under perfect asepsis 
and by the extraperitoneal route. For the first two days following the ligation the femoral 
pulsations disappeared but soon thereafter returned to normal. The animals were killed 
after varying periods of time and the vascular systems of both limbs studied with the X-ray 
after the vessels had been injected. The results of this study are summarized as follows: 

(1) The arteries below the ligation were found to be enlarged and to possess more 
numerous secondary branches than those of the corresponding area on the normal side. 

(2) There was no return of circulation in the tract of the external iliac artery at the end 
of one month but after two or three months a true collateral circulation had been established 
which was represented either by communicating arterial branches or by complete restora¬ 
tion of the segment of the main artery which had been excluded between the two ligatures. 

(3) The gluteal branches of the iliac artery, and especially these of the inferior or 
ischiatic gluteal artery, took part in the formation of the collateral circulation becoming 
larger and richer in branches. These branches anastomosed fully with the femoral 
branches. 

The results verify the theory as to the establishment of collateral circulation which was 
brought forward by Porta as far back as 1845. They demonstrate also that the increase 
in size of the preexisting collateral arteries is of greater importance than a very great 
increase of newly-formed vessels. This vascular dilation persists until the collateral 
circulation established is sufficient. 

It has often been pointed out that a congenital hypoplasia of the vascular 
system (sometimes cardiovascular) may be one of the predisposing factors 
that render certain individuals, possibly also certain races, susceptible to 
vascular affections. Indeed, for some of the vasomotor groups this theory 
has found adherents. So also, the hypothesis has been extended to the cases 
of organic vascular disease. 

Whether or not a congenital maldevelopment, implicating, therefore, 
possible collaterals as well, is influential in preventing the proper and ade¬ 
quate compensatory enlargement and dilatation of surrogate circulatory 
paths, is a question worthy of consideration. If vessels are inherently too 
small, it is not unwarranted to assume that when obliteration of important 
avenues of circulation interrupts the blood flow, the collaterals will become 
insufficiently developed and that gangrene may eventually ensue. 

From the anastomotic by-paths already existing, certain laws can be 
deduced as to the means of ascertaining the efficiency of the collateral circu¬ 
lation. If we study the course of these anastomoses and that of the palpable 
portions of the femoral and popliteal, we will learn that isolated compression of 
either vessel might give reliable information as to the circuit through which 
1 Bolognesi, G., Chir. a organi di movimenta, 1919, III, 4°3- 


84 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the collateral circulation travels. If, for example, we arrest the femoral 
artery at Poupart’s ligament, after having induced ischemia in the limb, 
either through an elastic bandage or prolonged elevation, and the circulation 
returns to the blanched parts in the pendent or horizontal position, we are 
warranted in concluding that a new source of blood supply has been estab¬ 
lished from a higher level. Such extensive central displacement of the point 
of influx is of rare occurrence. 

If the femoral and popliteal are patent and the latter is similarly tested, 
a positive flush or reestablished circulation would denote, too, that the col¬ 
laterals are adequate, arising above the level compressed. The anastomotic 
paths could'emanate then from any level between that tested and the femoral 
test point above. 

On the other hand, should color fail to return, the totality of arterial 
supply must be derived at and below the point at which the circulation was 
artificially arrested. 

Unfortunately, the femoral artery is not easily accessible to extraneous 
obliteration by compression except in its upper part, so that more accurate 
findings of the collateral niveau cannot be easily ascertained. Enough data, 
however, can be put at our disposal to warrant interesting deductions. 

If the test fails (circulation does not return after compression) at the 
popliteal level, certain prognostic inferences may be made, to wit, that a 
sudden thrombosis of this region would leave the distal parts without efficient 
by-paths. Conversely, those patients in whom the result is positive (circu¬ 
latory return) would offer a better immediate prognosis. 

With a positive test at the popliteal and a negative one at the common 
femoral, the intervening artery, in its totality, offers possibilities for ascend¬ 
ing blockage that must be compensated for by the remaining patent and cen¬ 
tral portion of its course. 

Demonstration of Collaterals in Obstructive Vascular Disease. —Some 

indications, as to the existence of effective new vascular by-paths can 
be obtained by compression of the femoral artery in the case of the lower 
extremities. Whenever chronic rubor is present, compression of the femoral 
artery for from 2 to 5 minutes may not suffice to efface the color of the foot 
in the diseased extremity, whilst similar compression on the healthy side pro¬ 
duces marked blanching {paradoxical ischemia on the healthy, paradoxical 
rubor on the diseased side). This would indicate that new interanastomoses, 
connecting points above and below the femoral artery, are more efficient in 
the diseased than in the healthy limb. 1 

The Course of New Channels. —The usual concept of these vascular 
by-paths is vague. All will concede their teleological significance—that they 
act as surrogates, devious, but nevertheless, purposeful avenues; and that 
through interanastomoses they succeed in delivering a sufficiency of blood 
even when large arteries are occluded. Little is known, however, as to 
the exact course along which the blood flows in any given case; whether the 
circulatory stream is shunted back again into an important vessel and thence 
to the periphery, whether altogether new routes are followed, or whether a 
combination of both exists. 

Perhaps it is not generally appreciated that, when ligation of an impor¬ 
tant artery is undertaken, the blood tends to seek and enter the main chan¬ 
nels again at some point beyond the occlusion. According to recent 
observations the task of the collateral is mainly to reestablish communi- 


1 See also tests for abnormal vasomotor reactions in thrombo-angiitis, Chap. LIV. 


COLLATERAL CIRCULATION 


85 


cation with the continuation of the main artery, and not to form a new 
arterial system of more extended course. 

When we speak of the collateral circulation in pathological conditions, 
we must visualize for ourselves the three factors upon which the new course 
of the circulation depends. These are: firstly, the situation of the most 
proximal point of obturation in the main vessel; secondly, the condition of 
the vessels beyond the central point of blockage—as to whether they are 
patent, narrowed (atherosclerosis, arteritis) or occluded (thrombo-angiitis 
obliterans); thirdly, whether the sudden advent of a centrally situated 
obstacle (obturation, ligation, thrombus, compression) is immediately or 
remotely followed by secondary stagnation, or accretion thrombosis in the 
arterial or venous channels. 

The problem of even vaguely appraising the direction of the collateral 
paths through existing anastomotic channels becomes difficult pari passu 
with the amount of impairment of the integrity of the arterial tree beyond the 
point of occlusion. Whilst it is easy to judge approximately as to the new 
current when a large artery is ligated, or when a small embolus is lodged and 
unaccompanied by secondary thrombosis in arteries that are healthy and 
patent, a very perplexing and intricate condition obtains when we are 
ignorant of the exact extent of a preexisting occlusion in the peripheral 
arteries. Therefore, in arteriosclerotic obturation and occlusion and in 
thrombo-angiitis obliterans, the sudden advent of thrombosis or embolism 
in larger more centrally located trunks offers a more dubious outcome, neces¬ 
sitates a more devious and circuitous route for the substituting arterial paths, 
and may make reestablishment with the former currents impossible. 

The Collaterals When the Peripheral Arteries are Patent. —The fre¬ 
quently accepted assumption that the ends of the extremities are in more 
imminent danger of gangrene, the nearer to the trunk the ligature is placed, 
is not in consonance with experience. And so it has been observed that one 
can tie off the axillary artery and the common femoral without much risk. 
Often the ligation of the femoral below the profunda is dangerous, while 
ligation of the popliteal artery is almost always followed by gangrene. 

In some investigations (Hotz) it was found that adequate collateral paths 
are in evidence, wherever large muscle masses require supply, and that at the 
insertions of muscles in the regions where transition into tendons occurs, 
there is but a sparse distribution of the arterial by-paths. 

In an attempt to explain two striking clinical observations on the frequency 
of gangrene after ligation at certain levels in the course of the main arteries 
of the lower extremities, some authors have concluded that the multitudinous 
smaller muscular branches are perhaps even more important than the larger 
and discrete anastomotic channels nourishing tendons, fascia and bone. The 
lack of development of muscular branches is given in explanation of the 
occurrence of gangrene, when the popliteal artery is ligated. The anastomotic 
channels about the knee (see Fig. 31), although apparently sufficiently large, 
do not seem to suffice when sudden occlusion of the popliteal artery occurs. 
On the other hand, when a process of slow development (such as tumor or 
aneurysm) has gradually diminished circulation in this region, the collateral 
paths may have become adequately enlarged. In these circumstances 
they are able to cope with the sudden emergency that arises when complete 
occlusion by thrombosis or ligation eventually occurs. 

The arteria profunda femoris has been considered important, for through 
its anastomoses with the pelvic gluteal and sciatic arteries, it may act to 
reestablish the current below its site of origin, when occlusion of the common 


86 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


femoral takes place. This explains the paradox that sudden obturation 
below the profunda may be even more dangerous than arrest of the circu¬ 
lation above its point of origin. 

A reference to Fig. 31 will recall the anastomoses about the knee joint known as the 
circumpatellar anastomosis or rete patellae. In this rich network are engaged vessels in 
the superficial fascia surrounding the patella, with branches to the patella, the knee-joint, 
capsule and neighboring muscles. The vessels partaking in its formation comprise: from 
above (1) the anastomotica magna from the femoral and the descending branch of the 
external circumflex; laterally, the internal (3) and external (2) superior, and the internal 
and external (5) inferior articular branches of the popliteal, and the muscular branches of 



IiG. 31. Schematic rough drawing of Fig. 32. —Schematic rough drawing of 

collateral paths about the region of the collateral paths about the region of the 
knee. ( Hotz ) elbow. {Hotz) 


the same artery; and from below, the anterior tibial recurrent. Although these vessels 
would apparently suffice as anastomotic channels, according to Hotz none of these give 
adequate supply to muscles. Merely the fascial planes, the tendinous insertions of the 
thigh muscles below, and the points of origin of the calf muscles above, are supplied with 
the tendons and capsules of the joints. These circumstances have been regarded as provid¬ 
ing an explanation for the danger of necrosis after ligation of the popliteal artery. 

In the case of the elbow (Fig. 32) similar conditions obtain. The superior profunda 
(1) by a medial collateral branch (3) anastomosing with the posterior ulnar recurrent and 
with the interosseous recurrent (7); and in front of the elbow establishing communication 
(4) with the radial recurrent (6); furthermore, the inferior profunda (2) or A. collateralis 
ulnaris superior, also anastomosing with the posterior ulnar recurrent (7) behind the internal 
condyle, while the anastomotica magna (3) makes connections in front of the internal 
condyle with the anterior ulnar recurrent; and posteriorly with the posterior ulnar and 
posterior interosseous recurrent. In view of the fact that these vessels not only supply the 
capsule of the joint and the tendons (as in the case of the knee) but take care of the circula¬ 
tion of large volumes of muscle, the contention of Hotz seems to be supported in the observa¬ 
tion that ligation of the brachial at the elbow may usually be carried out, without danger 
of gangrene. 0 
















CIRCULATION IN THE EXTREMITIES 


87 


. In the case of the shoulder region and upper arm, the paradox has been again pointed 
out that ligation above the circumflex arteries (anterior and posterior or their common 
trunk) is less dangerous than below that point. A reference to Fig. 33 clearly shows how, 
by anastomoses of the anterior circumflex with the acromial thoracic with the posterior 
circumflex and through the anastomoses of the posterior circumflex with the same arteries 
and the superior profunda (see 6 and 8 in Fig. 33), blood can be directly delivered from the 



Fig. 33.—Schematic rough drawing of collateral paths about the region of the shoulder. 

(. Hotz ) 

axillary and subclavian through these channels, through which, it may find its way again 
into the main artery below the point of ligation. When ligation takes place below the 
circumflex, a more devious route has to.be taken by the current. . Indeed, ligation below 
the origin of the profunda should be still more dangerous. Ligation high in the axillary 
may be borne by reason of the presence of the large vessels, the mammary, subscapulans, 
and long thoracic. 

Therapeutic Development of Collaterals— Methods for enhancing the 
circulation must necessarily include those that further the development of 
collateral channels. Intermittent compression of the femoral or brachial 
artery has been suggested, and is a procedure that may be of some value in 
the treatment of obstructive arterial diseases of the extremities. 


CHAPTER XIII 

CIRCULATION IN THE EXTREMITIES UNDER PATHOLOGICAL 

CONDITIONS 

CLINICAL MANIFESTATIONS 

There is no better teacher of the varied circulatory phenomena resulting 
from pathological conditions of the vessels of the extremities, than the clinical 
manifestations that shall hereafter be described. Careful observation and 
comparative appraisal of the normal and abnormal clinical manifestations 









88 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


are most illuminating. Through these we will more clearly appreciate the 
circulatory phenomena in diseases of various types and causation, than 
through theoretical and physiological considerations alone. Nevertheless, 
it may not be amiss here to dwell briefly on the more abstract questions, 
leaving their amplification, explanation and illustration for subsequent 
chapters. 

The interpretation of the phenomena of disturbed circulation meets with 
an abundance of pitfalls, if we do not carefully weigh the various factors that 
may enter into the resultant subjective and objective states. Although the 
blood supply of the extremities, and especially of their more remote portions, 
depends primarily on the size and patency of the arteries and veins, many 
other elements, both general and local may act to modify the abundance and 
rapidity of the flow of blood. We need hardly dwell upon the importance of 
the cardiac factor and general systemic condition, but shall confine ourselves 
to the agencies of more local source and effect. 

For example, a maldevelopment or hypoplasia of the peripheral vascular 
tree is a condition common enough to warrant serious consideration, both 
because peripheral nutrition suffers then more readily when vascular dis¬ 
ease is at hand, and also because of its vitiating action on the development 
of adequate collateral channels. The presence of such an inherent anat¬ 
omical mediocrity or inferiority must be deemed possible in any given, case, 
and its participations carefully weighed in every instance of failing local 
circulatory compensation. Just as aplasia and anomaly must be con¬ 
stantly kept in mind when the clinician makes a critical appraisal of any 
given case of surgical renal lesion, so here too, one must not lose sight of the 
factor of congenital hypoplasia. 

The multitudinous distribution of the vessels,, their variation in capacity, 
their subserviency to alterations both of organic, functional and neurotic 
nature, allow of kaleidoscopic combinations of manifestations. 

The effects of obstructive lesions will be distributed, in a measure, over 
the area supplied by the vessel or vessels involved. But only with this reser¬ 
vation, to wit: that these effects are limited in intensity and in extent by 
time and the possibility of substitutions through other circulatory avenues. 
So, whilst the quantity of blood and rapidity of flow may be objectively 
and subjectively manifested in certain areas of the normal distribution at a 
time immediately following the advent of a sudden arterial obstruction, the 
intervention of preexisting and later of compensatory collaterals, is responsi¬ 
ble for partial or complete disappearance of all phenomena. 

Serious alterations (in the vessel integrity) may have as their consequence, 
no appreciable manifestation other than those of diminished blood supply, 
decreased warmth and slight sensory disturbances. But where a large 
territory is affected, by virtue of the exclusion of more central, more impor¬ 
tant and larger arteries, or through a larger number of arteries, associated 
effects may be then evoked. These are: 

(1) Immediate effects; or the residual changes persisting after rehabilita¬ 
tion of the circulation. 

(2) The induced or reactionary processes in the peripheral capillaries 
and arterioles, viz. rubor, hyperemia, or erythromelia. 

(3) The tendency to trophic derangements. 

(4) The production of either transitory or permanent lability of the local 
vasomotor mechanism. 

Whereas both subjective and objective signs of a suddenly interrupted or 
seriously disordered circulation in a given territory are usually definite and 


CIRCULATION IN THE EXTREMITIES 


89 


vivid enough to be both experienced by the affected person and easily recog¬ 
nized by the physician, the slower and more gradual obstructive lesions of 
the vessels may be easily overlooked. And so, it has been clinically proven 
that insidious, progressive occlusion of main arteries of the lower extremity, 
including the femoral, popliteal, posterior and anterior tibial arteries, may 
take place without symptoms; and, indeed, the clinician may fail to recognize 
the basic vascular lesions until gangrene or trophic disorders follow a slight 
trauma or local infection. As shall be pointed out later, however, certain 
objective signs can be usually elicited, and careful examination will lead 
to the discovery of the condition long before grave consequences ensue. 

The subjective appreciation of local deviation from the normal must 
needs vary with the individual’s apperception and introspective psyche, as 
well as with his threshold of sensitiveness. Our interrogations, therefore, 
should be so put as to make up for the deficiencies of those who might lead 
us astray. Pain in the affected territory, coldness, paresthesia, liability to 
fatigue, may antedate by months or years, the appearance of the more 
easily recognizable features. Coldness of the toes of spontaneous onset, or 
after but slight degrees of exposure, is also a sign worthy of note. It must be 
remembered, however, that pari passu with the gradual extension of the 
vascular obturation, collateral paths may enlarge so that subjective symp¬ 
toms may disappear. On the other hand, the liability to pain and cramps on 
walking may increase as time goes on, and masquerade under the guise of 
rheumatic pains, flatfoot ache, “cramps from varicose veins” and the like. 

The signs that may be objectively elicited will be discussed in full elsewhere. 
They include (i) the immediate result of circulatory inadequacy; (2) the 
evidences of dilatation of peripheral capillaries and arterioles (rubor or 
erythromelia); (3) vasomotor lability or instability; and (4) trophic dis¬ 
orders and gangrene. 

In the interpretation of the prognostic significance of these manifestations, 
we must bear in mind their intensity and extent, the duration of their exis¬ 
tence, their constancy and especially the progressive nature of the phenomena 
of malnutrition. The immediate results of circulatory impairment may, 
as already mentioned, be so slight as to escape notice. With sudden and 
extensive interruptions of the current, however, pallor of the foot (or even 
leg) on walking, on elevation, or in the horizontal position, is a significant 
sign. Coldness of peripheral parts to the touch, with a distinct increase in 
warmth of portions more centrally located, is an important objective phe¬ 
nomenon. Other expressions of nutritive disorder include those more 
delicate changes in the skin texture, the nails and the subcutaneous tissues 
that are to be described in detail. 

The condition of rubor (erythromelia) is such a characteristic manifesta¬ 
tion as to warrant careful and detailed study. It may develop very gradually 
or within a very short time; it may be a permanent sign or gradually dis¬ 
appear; and is under the influence not only of the immediate state of the 
circulation of the part, but also dependent on posture. 

Vasomotor instability is not a constant attendant disturbance, although 
well marked in some cases. Its expression may lead to confusion, and there¬ 
fore, its role and its separation from evidences of purely hydrostatic or 
mechanical origin may be occasionally difficult. 

Trophic lesions and gangrene, too, are characteristic results of poor local 
nutritive states. However, even the causation of these may not be altogether 
clear, whenever signs of apparent vasomotor lability seem to dominate the 
picture. Of the less striking, but nevertheless important effects of these 


90 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

maladies, are the alterations in deeper tissues, particularly of the bones. The 
changes in conformation of visible parts give us a clew as to abnormalities in 
the subcutaneous tissues. But the condition of the bones requires elucidation 
with the Roentgen ray wherever there is a doubt as to diagnosis. It is 
noteworthy that the osseous tissues may suffer even greater absorption in 
some of the true vasomotor neurogenic circulatory disorders than from the 
more constant effects of organic vascular occlusion. 

Evidences of disturbed nutrition may be hyperplastic rather than degen¬ 
erative. And so hypertrophy of the subcutaneous tissues is occasionally 
seen with chronic cyanosis of the hands. 1 

In the neurogenic or vasomotor derangements, sensory and objective 
circulatory phenomena may be so closely linked in onset and duration, that a 
causal interrelationship is often assumed to exist. The effects of the purely 
hydrostatic depletion, stasis or deficiency of flow (through vasoconstriction) 
are here also hard to separate from trophic disorders attributable to pure 
neurotrophic abnormalities. In short, whereas in organic occlusive disease 
of the arteries, a direct association between trophic disorders and circulatory 
insufficiency can usually be invoked in explanation, the nutritive complica¬ 
tions of the vasomotor affections, may be under the influence of one or several 
different forces. 


CHAPTER XIV 

THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM 

The role of the nervous system in the production of trophic disturbances, 
wounds that refuse to heal, ulcers, necroses and gangrene should be 
thoroughly understood as far as present day knowledge permits, in order that 
the clinician may differentiate the neurogenic cases from those of organic 
vascular origin. When we speak of trophic disturbances, we can, in a broad 
way include not only those that are directly dependent upon poor circulation, 
or the action of external insults (cold, chemicals, heat, etc.), but also some of 
the clinical effects of nerve derangement. Classification is made difficult by 
reason of the fact that we are at pains to conclusively differentiate between the 
trophic lesions produced by external and endogenic causes. Some believe 
that severe cold may produce its effects only by direct action, and others 
attribute the tissue disturbances for the most part to the neuroparalytic 
effects of cold upon the blood vessels. For our purposes, it would be well to 
keep in mind two large categories; trophic disturbances of a nutritive or mal- 
nutritive nature from whatever cause, and those of purely neurotrophic 
origin. 

Several theories have been put forth to explain neurotrophic disorders 
in the peripheral tissues; firstly, that the inflammation extends along the 
nerve until the innervated area is reached; secondly; that the inactivity 
induced by the neurogenic condition is responsible; and thirdly, that the 
anaesthesia produced by the nerve lesion results in an inability to avert 
injury. Numerous clinical observations, however, have shown that none of 
these causes must obtain. We are, therefore, constrained to accept the view 

^ee Chap. XCV, page 528. 



91 


THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM 

that there is a direct trophic influence exerted on the tissues through the nervous 
system. 

The Exercise of Neurotrophic Influences. —Several theories have been 
offered in explanation of the paths along which trophic influences are exer¬ 
cised. 

One vasomotor theory presupposes that the tissue changes depend upon 
vasomotor influences. Accordingly trophic lesions may result from neuro¬ 
paralytic hyperemia, or from anemia due to neuro-irritation. 

The theory of neuroparalytic hyperemia is based upon the supposition that in these 
circumstances, inflammation and nutritive disturbances occur more easily than with a 
normal vascular tone. Certainly experiments do not corroborate this theory; in that ten¬ 
dency to inflammation through experimental lesions of the sympathetic in animals has not 
conclusively shown increased tendency to inflammation. 

The theory (Brown-Sequard) that a nemo-irritative ischemia is responsible 
for certain trophic disturbances also has not found substantiation. Of recent 
years some of the European authors have attributed late trophic disturbances 
in gangrene (after exposure to cold) to neuroparalytic lesions of the blood 
vessels. 

It does not appear proven nor plausible that either vasomotor theory should account 
exclusively for trophic disturbances. Alterations in the blood content of the affected part 
have not been observed clinically to precede the trophic disturbances, except in those cases 
(thrombo-angiitis) where the nutritive lesions can be explained otherwise. Certainly 
in the neurotic muscular atrophies or in the neurotic glandular atrophies, or in the tabetic 
arthropathies, no such prodromal vascular disturbances have been noted. In short, vaso¬ 
motor derangements can only be regarded as contributory causes. 

The Theory of Special Trophic Nerves. —According to another hypothesis 
special trophic nerves are assumed to exist (Samuel 1 ). Perhaps the only 
affection which presents symptoms that would seem to substantiate such a view 
is that called progressive facial hemi-atrophy. 

This is a disease in which the skin, as well as the bones of one side of the face slowly 
atrophy. According to Samuel this condition is to be attributed to an isolated lesion or 
paralysis of trophic nerve fibers. However, in almost all such cases other nervous derange¬ 
ments of sensory and secretory type, are present. The implication of other nerves, particu¬ 
larly the trigeminal, and in some cases also the sympathetic, are facts that warrant a 
modification of the above hypothesis and do not permit of the wilful assumption that 
specialized trophic paths are present. 

In short, the existence of isolated special trophic nerve paths and centers 
has not been proven clinically or experimentally. Most observations and 
investigations, therefore, agree in supporting the conclusion that the trophic 
influences pass through the very same nerve paths and centers that possess 
other special function. 

As to how the trophic influences act, a number of different theories have 
been advanced, and perhaps it is best to discuss these in connection with 
the different tissues, since their actions may not be uniform, and then to 
point out in what form and to what extent these tissues are subject to such 
trophic influences. Of these theories, there are those that presuppose a diminu¬ 
tion in nervous influences; others that interpret the trophic influences as 
conditions of irritation or excitations; and finally those according to which 
trophic lesions depend upon abnormal reflex stimuli from the periphery . 

Closed Circuit and Nerve Impulses. —It is still a mooted question as to 
whether direct contact of nerve elements is necessary for the exercise of 
nervous forces. 

1 Samuel, Trophoneurosen, Eulenburgs Realencykl., XX, II, Aufl. 


92 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The Interdependence of Nerve Paths with Particular Reference to Trophic Function— If we 
accept the neuron theory, we believe that the nervous system is made up of innumerable 
nerve units or of anatomically or physiologically specially destined and characterized indi¬ 
vidual cells. The constituents of such units are the cell bodies with their dendrites, their 
nuclei and nucleoli, and the axis cylinders, the latter leading into medullated or non-medul- 
lated fibers. According to the new tinctorial methods that show fibrils in the axis cylinder, 
the histologic unity of these nerve cells and their processes has been subject to strong criti¬ 
cism. These fibrils appear in the axis cylinder as long, parallel lines or threads, whilst they 
split up in manifold fashion in the ganglion cells, intersect and intertwine. Besides these the 
neurofibrils pass from one dendrite of one cell into its neighbor’s. 

We are still uncertain regarding the manner in which communication 
takes place between the intracellular neurofibrils, and those peculiar and 
varied endings of nerve fibers that approach the cells from the nerve fibers. 
We should not hold too tenaciously to the concept of an anatomical independ¬ 
ence of the nerve units. 

Be this as it may, the transmission of the nerve impulses from the phy¬ 
siological standpoint from one cell to another can be carried out by nerve 
streams that pass directly or through a gap; and it appears irrelevant as 
to whether direct communication is present or not. 

As for the role of the nerve cells in the production of trophic influences, some authors 
have regarded those ganglia cells that are included in the heaps of fibrillar substance as 
having no other specific function than that of nutritive reservoirs. There have been but 
very few adherents to this special doctrine. 

The Interdependence of Certain Portions of the Nervous System as Studied in Nerve 
Degeneration.— Three types of degeneration occurring in the nervous system throw con¬ 
siderable light upon their function and anatomy. These may be divided into the Wallenan 
degeneration, or Lenhossek cellifugal degeneration, the retrograde degeneration, and 
secondary atrophy or indirect degeneration. 

i. The Wallerian Degeneration. —Section of a motor nerve is followed by degeneration 
distal to the point of the break in continuity and up to its endings in the muscle. Section of 
a sensory nerve is followed by degeneration up to the endings in the periphery. Section 
of a posterior root causes degeneration of the intramedullary course. Therefore, the 
degenerative process is always away from the cell (cellifugal) in the sense of the physiological 
direction of the impulses (towards the periphery, or caudad). It appears that the neuron 
theory gave a satisfactory explanation of the destruction of the axis cylinder, when severed 
from the cell, the accepted belief being that the neuron constitutes a nutritive entity. It is 
hard to conceive, however, how parts situated at great distances from the cell can obtain 
their nourishment through it. Indeed, the nodes of Ranvier have been regarded as points 
of entrance for nutritional fluids. Therefore, the trophic action of the nerve cell must be 
interpreted in another light, possibly as exerting such influences on the axis cylinder that 
enable it to attract nourishment from the neighborhood, and utilize it. The assumption 
that a ferment substance emanates from the cell, gives no more satisfactory explanation 
than the view that centrifugal impulses from the cells assure the axis cylinder of the power 
of nutritive assimilation. Furthermore, we cannot adhere too strongly to the notion that 
trophic influences are confined merely to an anatomic unity of the cell and its axis cylinder. 
The observations upon which the whole theory is built up do not concern themselves with 
single cells and their processes, but in fact we are always dealing with a multiplicity of cells 
and fibers. When we speak of degeneration clinically and anatomically, also pathologically, 
cell groups and fiber groups only are actually considered. 

Concerning the dependence upon central nerve matter and peripheral fibers, observa¬ 
tions are at hand that show that lesions in the spinal cord follow in the wake of amputation. 
For instance, distinct alterations in the spinal cord not limited to the white matter, 
but implicating the ganglion cells with diminution in size of the anterior gray horn have been 
observed. Involvement of the anterior or posterior tract and varying amount of implica¬ 
tions of the white and gray substance have been observed. 

Theory of Cellular Excitation .—According to Monakow it would appear 
that alterations in the ganglion cells, after section of the peripheral nerve, 
depend upon two factors: firstly, as to whether the cell is in possession of 
rich collaterals; and secondly, on the point of section. When the point of 
section is very far removed from the cell, its action is minimal as compared 


THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM 


93 


to proximal interruptions. The degeneration of the cell, in his opinion, 
would depend rather upon the amount of functional disturbance. The 
degree of disturbance of the latter is directly related to the number of func¬ 
tional impulses that are excluded, these including not only influences from 
the axis cylinder itself, but of all the neighboring nerves that are in close rela¬ 
tion to it. Perhaps all cells require similar stimuli for the conservation of 
their trophic integrity. 

Section of axis cylinders causes rapid changes in the related anterior horn and ganglionic 
cells in most cases. 

The intensity of these changes vary, and the cell may undergo a reparative process, a 
return to the normal occurring to a considerable extent. Whenever the cut nerves become 
reunited, the cells return to normal. Per contra, these undergo simple atrophy when the 
function is in abatement by reason of a permanent break in continuity. 

2. Retrograde Degeneration .—In this category belong the degenerative processes that 
manifest themselves in a reduction of the size of anterior root fibers after amputation. 
Similar narrowing of the posterior root leading into the posterior tract has often been 
observed. Then, too, diseases of the peripheral nerves, either peripheral neuritis or the 
action of compressing tumors, is followed by some degeneration in the corresponding pos¬ 
terior roots and the corresponding posterior tract. Although in some cases these changes 
have been interpreted as an extension of the toxins that led to the polyneuritis, in other cases 
the changes have been believed to be of reactive nature in consequence of the peripheral 
lesions. Such apparent retrograde degeneration is not confined to the territory of the 
motor and sensory nerves. They have been found in the brain itself and in the centers of 
the optic thalami after cortical lesions. 

The Reflex Theory. —Explanations of so-called retrograde degeneration 
throw important light on the problem of trophic influence of the nervous 
system. According to one view, the trophic functions of the nervous sys¬ 
tem are not automatic, but reflex in nature. Marinesco expressed the 
following hypothesis, in explanation of the central proximal atrophy occur¬ 
ring after amputation. The cause of the degeneration (in the cells and in 
the central stump) is to be sought in the interruption of the continuity 
between periphery and center. One may suppose that by irritation of the 
sensory nerve endings biologic changes (probably of chemical nature) are 
produced in the spinal ganglia, and that a trophic influence in the efferent 
fibers from the ganglionic cells is thereby exerted. When section of an 
extremity or of a nerve takes place, quantitative and qualitative changes 
in the impulses through the nerve ends must needs result that are no longer 
able to evoke the adequate trophic function; therefore, a slow progressive 
degeneration of the nerve fibers ensues. Just as the fibers of the central 
nerve stump show changes, so also the fibers which travel from the spinal 
ganglia to the spinal cord become altered. This explains the atrophy in 
the sensory sphere. According to this view, impulses travelling to the cells 
simultaneously serve to conserve their trophic function. 

According to a supplementary view, such activating nerve stimuli do 
not necessarily have to emanate from the periphery, but may be of central 
origin. That is, other reflex impulses that are subconscious may be effec¬ 
tive. Among these may be mentioned metabolic processes, emotion, and a 
variety of constantly changing and repeated, almost continuous stream of 
impulses of sensory and motor nature. These serve to excite the trophic func¬ 
tion of the cells , and when absent, there result those atrophic alterations of 
the ganglion cells and their processes that have been observed. 

According to still another interpretation, it is the inability to give off impulses that is 
the essential factor in the production of the degenerative cell changes (Lenhossek). For the 
conservation of the normal integrity a continuous function of the cell is necessary. 


94 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


That section of the posterior root is followed by degeneration of the spinal ganglionic 
cells is difficult of explanation. Under such circumstances, impulses are still received, and 
in spite of this fact, marked derangement in the anatomical conditions of the spinal gan¬ 
glion cells is noted. From this we would have to conclude that an uninterrupted flow 
of impulses from the cells or the cell responses, is essential for the conservation of the cell 
equilibrium. Every derangement of function, be it an obstacle to the reception of impulses 
or changes in the giving off of impulses leads to alterations in the anatomical structure of 
the nerve cells. Unfortunately this theory is nothing more than another way of stating 
the facts. 

The Theory of Heterologous Stimulation .—Interferences with trophic 
function are said to be also due to suppression of impulses in neurons that 
are not in anatomical but in functional relationship. Observations on 
secondary atrophy would substantiate such a view. 

3. Secondary Atrophy or Indirect Degeneration. —Under this name, Monacow describes 
secondary changes in the nerve fibers and ganglion cell groups characterized by qualitative 
conservation of the histologic elements, but distinct diminution in volume of all parts. 
The medullary sheath becomes very narrow, very thin, the nucleus poor in chromatin and 
the Nissl bodies of the protoplasm become indistinct. 

This degeneration has been explained on the assumption that through the suppression 
of one neuron, changes take place in a second neuron that is functionally in relation with the 
first. As an example may be mentioned the amyotrophic condition in tabes following 
disease of the sensory protoneurons. So also Schaeffer would explain the changes in the 
anterior horn cells as due to disease of the sensory neurons. 

According to this view, trophic derangements extend not only through 
homologous (motor-motor) but also through heterologous (motor-sensory) 
neurons. The condition of certain nerve fibers is doubtlessly influenced 
from the trophic standpoint, through systems that are in close functional 
and anatomical relationship. 

In short, the striking peculiarity of the nervous system is the interde¬ 
pendence and relationship between function and structure of the cell. The 
function consists of the reflection of the impulses or irritations, the elabora¬ 
tion and the conversion of the irritant or impulse, and finally the giving off 
of impulses. It is even possible that disturbances in any one of these three 
functions may lead to localized trophic disorders. On the other hand, it is 
doubtful that the integrity of any unit is absolutely essential for conservation 
of its nutritive condition. Indeed, the neuron theory does not explain either 
the so-called retrograde degeneration, nor the secondary atrophy. Cassirer 
believes that if we consider the ganglion cells as a sort of center, that is in 
spatial and functional relationship with a certain number of degeneration and 
trophic disturbance, as upon the basis of the unity of the ganglion cell and 
its processes. 

Nerve Influences on Osseous Tissues. —A few words concerning the 
dependence of the conservation of bony tissue on nerve influences may 
not be amiss, since trophic alterations, particularly in the end phalanges 
can give us valuable diagnostic information. The differentiation of pri¬ 
mary atrophy of the distal phalanges associated with Raynaud’s disease 
and sclerodactyly from nutritive disorders due to inactivity, syphilis, 
syringomyelia and secondary infection may be thereby facilitated. 

The nerve control of osseous nutrition is well exemplified by the retarded bone growth 
of infantile spinal paralysis. There are also some clinical observations on disturbed growth 
of bones after peripheral nerve lesions. Gayet and Bonnet described a case in which resec¬ 
tion of a neuroma formation in the median nerve seven years previously was followed by 
diminution in size of bones and rarifaction. A number of instances of intensive osseous 
changes after traumatic lesions of peripheral nerves can also be found in the literature. 


THE TROPHIC FUNCTIONS OF THE NERVOUS SYSTEM 


95 


Bone disease associated with diseases of the central nervous system is 
more common. In syringomyelia, osseous alterations are not infrequent. 
These are necroses particularly of the tips of the phalanges of the fingers, 
or diminution of their size; or, even disappearance of small bones without 
inflammation or suppuration. Roentgenograms may show bone atrophy 
and lightening of the bone shadows, both of the diaphysis and epiphysis. 
Even enlargement of bones has been reported without the presence of 
acromegaly in cases of glia changes in the spinal cord. 

Fragility of bones, too, occurs in paralytics, although this has been 
interpreted by some as due to atrophy of inactivity. A rarifying process 
may make the bones brittle when tabes is present, and liable to spontaneous 
fracture. 

There are cases in which after trauma of an extremity without wound or 
suppuration, marked trophic disturbances appear. These may be accom¬ 
panied by slight vasomotor symptoms and sensory irritative phenomena, 
but deficiency manifestations in the sensory nerve domain are absent. 
Here it is believed that the trophic disturbances have a reflex cause through 
excitation of the sensory apparatus. Cassirer mentions a case of Sudeck 1 
in which after injury of a hand, swelling, redness, pain and restricted motility 
resulted. The X-ray picture presented the characteristics of bone atrophy 
with clarified bone substance and typical atrophic changes in the carpal 
bones. Even osteophytes are said to occur as an expression of continued 
reflex irritation. 

Characteristic in lepra are the resorptive and degenerative processes in 
the peripheral phalanges with mutilation of the parts. The lime disappears 
hand in hand with atrophy of the rest of the bony parts, and corresponding 
changes in the soft parts. The bony resorption in these cases is so character¬ 
istic and so extensive, that it can hardly be mistaken either for the very 
minimal changes of Raynaud’s disease or sclerodactyly; nor can it be readily 
confused with the bone and joint destruction associated with perforating 
ulcer, arteriosclerotic ulcers and gangrene. 

The cause of the bony changes is said to be a trophoneurotic one due to 
lesions in and about the peripheral nerves. 

Trophic Influences on the Vessels. —If such a relationship exists, it is all 
the more important by reason of the secondary effects that could be thereby 
transferred to the tissues supplied by the vessels in question. Lapinsky 
claims to have demonstrated structural changes in the walls of arteries after 
section of the vasomotor nerves. Cassirer accepts the experimental work of 
this author as reliable even though others (Jores) could not offer confirmatory 
facts. 

As for the manner in which vessel alterations are dependent on the vasomotor nerves, 
satisfactory explanations are difficult to find. In how far do these changes result from the 
absence of functional impulses? Or, to what extent are direct nutritive stimuli responsible 
for conservation of anatomical integrity? A complicated mechanism is put into action 
when vasomotor nerves are experimentally cut off. For, the induced dilatation of the 
vessel permits of new mechanical hydrostatic or circulatory forces to come into play and 
possibly exert an effect on the arterial walls. Perhaps the therapeutic results of future 
operations on the periarterial sympathetic fibers (Leriche) will throw additional light on 
this obscure subject. 

1 Sudeck, Monatschr. f. Unfallheilk., VII, 50, 1910. 


96 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XV 

TROPHIC DISORDERS OF THE SKIN 

Neurotrophic disorders of the skin include all those regressive, hyper¬ 
trophic, and so-called inflammatory changes dependent upon the nervous 
system. The skin and the nervous system are brought into communication 
through those sensory nerves in which fibers of the cerebrospinal and vege¬ 
tative systems are contained. Probably the sensory nerves per se have no 
direct influence upon the vital functions of the skin. When the sensory 
paths are interrupted, the parts are placed in jeopardy, insofar as injurious 
moments do not come to consciousness. Such is the case in syringomyelia 
and in interruptions in the continuity of the peripheral nerves. As a rule, 
trophic changes associated with sensory disturbances depend exclusively 
upon lesions or irritations of the vegetative nervous system, whose paths and 
centers are in intimate relationship and contact with the sensory fibers. 

The distribution of blood, and therefore the nutrition of the skin, is under 
influence of the nervous system through the vasomotor paths. And so, a 
continued spasm of vasoconstriction and so-called neurogenic stasis may cause 
functional derangement of the skin. 

The immediate effects of injury of the peripheral nerves demonstrate 
that the cutaneous vessels may functionate independently of the nervous 
system. Later on, however, distinct disturbances in the blood supply 
appear, such as anemia or cyanosis; and with this, other changes in the surface 
of the skin, namely, purplish discoloration, thickening, changes in the nails 
and glossy skin. The latter are evidences of dystrophic or maltrophic altera¬ 
tions in the integument. And so also, the vascular responses to external 
stimuli or conditions suffer a change. Under such circumstances there is 
a tendency towards severe regressive or degenerative changes. Inflamma¬ 
tory processes are intensified and the ability to heal is diminished. 

In addition to the vasoconstrictor and dilator paths, vasosensory fibers 
course in the peripheral cutaneous nerves. They are important in the nutri¬ 
tion of the skin. For we can only then expect an orderly nervous regulation 
of the blood distribution when a harmonious and reciprocal association of 
the vasomotor and vasosensory impulses obtains. 

According to some it is hardly necessary, nor in accord with any observa¬ 
tions to postulate the existence of a separate trophic nervous system. In 
cases of nerve lesions trophic disorders may be absent for years. The origin 
of the so-called glossy skin has been explained upon the theory that the vaso¬ 
motor relations have been disturbed. A thickened, brittle skin with hyper¬ 
keratosis is also noted in cases of peripheral nerve lesions and in localized 
spinal diseases, such as syringomyelia. 

Of the so-called inflammatory types of trophic disorders herpes zoster is 
an example. This is the only one of the trophic disorders in which certain 
distinct anatomical changes in the nervous system have been demonstrated. 
There are hemorrhagic inflammatory processes in the spinal ganglia. 

Certain cases of circumscribed edema and urticaria may be of neurogenic 
origin, whilst in other cases a toxic cause is responsible. That neurogenic 
cases can exist is proven by the examples of urticaria of psychogenic or reflex 
creation demonstrable after the passage of bougies in the urethra; and also in 
dermatographism. The exact nature of the responses depends to a consider¬ 
able extent upon the predisposition of the skin, and upon the individual. 


TROPHIC DISORDERS OF THE SKIN 


97 


Trophic disorders of the nails manifest themselves in irregular growth. 
The nails may become plump, easily torn, show furrows, may degenerate, 
and later may break up. External injuries or insults often give rise, in 
predisposed individuals, to inordinate responses on the part of the skin. 
Such a predisposition to trophic disorders is exhibited by certain weak cuta¬ 
neous structures in cases of myelitis or nerve injuries or lesions. 

A number of skin lesions have been regarded as due to trophoneurotic 
causes. Amongst these may be mentioned: malum perforans, acute decubi¬ 
tus, skin changes of peripheral nerve disease, and those associated with syringo¬ 
myelia. All of these should be carefully studied before we can possess 
correct diagnostic appreciation of the varied clinical pictures of gangrene. 

Mai perforant is fully discussed in Chap. LXXXIII. To what extent 
this process owes its character to nerve lesions has not as yet been con¬ 
clusively proven. In some cases at least we may accept the existence of 
derangement of sensory nerves as well as of vessel reflexes. 

As for acute decubitus, views differ as to the role of mechanical infectious 
or neurogenic influences in its causation. A careful perusal of the literature 
permits us to cull a few authentic examples of undoubted neurogenic nature. 
In such the skin necrosis is said to have developed a few hours after the onset 
of the nerve disturbance (hemiplegia and hemianesthesia). That immediate 
skin changes can follow cerebral lesions is recorded in the reports of pemphigus¬ 
like eruption in the paralyzed areas, extensive bleb formation in territories 
with sensory and vasomotor disturbances, etc. In some cases “decubitus” 
is the product of a combination of factors, pressure, vasomotor weakness of 
the skin, and infection. 

Another manifestation of the relation of the nerve and cutaneous systems, 
is the glossy skin described by Weir-Mitchell. Not greatly dissimilar are 
some of the remarkable changes in the integument occasionally seen in the 
feet, when slowly progressing but vast arterial obstructive lesions of arterio¬ 
sclerosis impair the nourishment of the parts. Also, in rare cases of throm- 
bo-angiitis obliterans, a condition of the skin of the hands, with trophic 
lesions of the nail beds, without ulceration, may give deceptive pictures. 

In glossy skin the skin is red, thin, shiny and stretched. With it there 
may be burning sensations or neuralgic pain. The hair and rugae of the 
skin may be absent, whilst sensation may be conserved. It is important 
to note that this lesion appears when only partial section or interruption of 
nerve continuity in the territory has taken place. 

If the cutaneous disturbances correspond to the territory innervated by 
certain nerves, their neurogenic nature is usually easy to recognize. 

A word may not be amiss regarding neurotrophic skin changes attending 
syringomyelia, which must also be occasionally considered in differentiating 
trophic disorders and gangrene. Here the lesions] are usually associated 
with motor, vasomotor and sensory derangements. Nor can we always 
establish a causal relationship between the cutaneous changes and other 
evidences of nerve lesion, since the former may antedate the latter. 

As for other lesions, such as herpes zoster and multiple neurotic gangrene 
of the skin, these would seem to indicate the existence of a close neurotrophic 
relationship. In the case of herpes, Head says that the eruptions are not 
produced by disturbance of special trophic nerves, but by intense irritation of 
cells in the ganglia, which normally subserve the function of pain. Probably 
irritation of sensory end-neurons are responsible for the trophic changes in the 
skin. Cassirer suggests a reflex disturbance of the vasomotor nerves through 
sensory impulse. 

7 


98 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In multiple neurotic gangrene of the skin such vasomotor derangement 
has also been considered possible, the reflexes being either of toxic, electric 
or psychic nature. 

The so-called trophedema is a hard, white, painless edema of rather 
chronic course. It is usually observed in youth and is progressive.. It is 
demarcated by a sharp circular line in a segmental fashion, being limited to 
certain parts of the limb, and is not infrequently a familial disease. 

Pathogenesis of Neurogenic Gangrene. —The question as to whether 
gangrene may result solely from changes in, or functional derangement of the 
nervous system without reference to effect of vasomotor spasm, has been a 
much mooted one. As for the peripheral nerves, evidences are lacking that 
these are the seat of degenerative changes either in Raynaud’s disease or in 
other cases of spontaneous neurotic gangrene. When they are reported as 
having been present, they are usually not the cause of the gangrene, but sec¬ 
ondary, and result from the same forces that are productive of the gangrene. 

As regards the central nervous system, it is known that marked nutritive 
disturbances of the skin and its adnexa can be associated with the central 
nerve changes, as in syringomyelia. Indeed, gangrene has been observed 
complicating even gliosis. 

Cassirer is unwilling to accept the purely ischemic theory or that of 
angiospasm as sufficient to explain the gangrene in Raynaud’s disease. This 
view receives additional confirmation in the manifestations of gangrenous 
herpes and in the disease of multiple neurotic skin gangrene , where irritation of 
the vasomotor nerves is believed to occur. Indeed, Kreibich 1 was able to 
produce angioneurotic inflammation experimentally, and also, patches of 
gangrene in the latter affection with the use of faradic current and other 
irritants. He suggests that the nerve impulses excite paralysis of the vessels 
through irritation of the vasodilators with consequent edema, exudation, and 
necrosis; and that the necrosis is due to increasing pressure of the exudate. 

These observations, however, cannot be invoked in explanation of the 
Raynaud complex, since, in the latter, vasoconstrictor, and not vasodilator 
irritation exists. Whilst Kreibich and others would interpret the necrosis 
as the result of mechanical effect of an exudate of vasomotor origin, Cas¬ 
sirer rejects this assumption, believing it more plausible that there is a direct 
trophic action through the nervous system on the tissues; and with such a 
theory he would interpret gangrene associated with both vasodilator (multi¬ 
ple neurotic gangrene) and vasoconstrictor (Raynaud) impulses. Enough 
data are at hand, however, irrespective of which view may be correct, to 
warrant the belief that neither angiospasm nor ischemia satisfactorily accounts 
for all types of neurogenic necrosis or gangrene; for this occurs where vaso¬ 
dilatation has been shown to exist. It may be accepted therefore, that a 
primary gangrene of the skin may take place by reason of alterations in, or 
functional derangement of the nervous system. 

A new French school has arisen that would regard even trophic ulcers of traumatic 
peripheral nerve origin as explicable by the theory of deranged vasomotor function. Thus 
the trophic ulcers complicating transverse injury of the sciatic nerve 2 have been recently 
attributed to vasomotor reflexes produced by a neuroma of the nerve’s proximal end. Ac¬ 
cording to this theory the active proliferation in the neuroma is the point of departure of 
vasodilator reflexes that augments the existent circulatory disturbances. By virtue of 
this effect minimal local peripheral traumata may give rise to sero-sanguinolent exudation 
in the connective tissue meshes, in which the dilated capillaries have lost their function 
and that consecutive cutaneous necrosis and ulceration ensue. 3 

1 Kreibich, Die Angioneurot. Entziindugen, Wien, 1905. 

2 See Chap, on Trophic Disorders in Diseases of the Peripheral Nerves. 

3 Leriche, Lyon Chirurg., 18, 1921, p. 43-44. 


TROPHIC DISORDERS OF THE SKIN 


99 


Summary. —The passive tissues too, such as skin, bones and joints, are 
under the control of trophic nerve influences. It would seem that a specially 
attuned reflex mechanism is here essential for the harmonizing of their nutri¬ 
tional condition and their specific functions. Cassirer offers the following 
views: Pathologic changes of innervation exert a more injurious effect on 
the nutrition of tissues, than when nerve impulses are completely in abeyance. 
Excitation of sensory nerves calls forth marked reactions in vascular inner¬ 
vation. Although the tissues, in general, are trophically innervated, they 
may continue spontaneously to make up for nutritive defects. The special 
trophic impulses would only then be significant when the nourishment of the 
tissues is under special strain, as in the presence of unfavorable conditions 
such as continued pressure, and unusual desiccating influences. But when 
the normal innervation becomes pathologically altered through special 
irritants, the nourishment of those tissues that are within the anatomic and 
physiologic boundaries of the exciting impulses, may be reflexly modified 
thereby; and as long as the special irritants continue. So that accordingly 
it is not an absence of innervation, but rather a pathologically deranged form 
of nerve impulse that comes into consideration in the development of trophic 
lesions. Indeed Leriche has recently expressed the hypothesis that trophic 
ulcers after nerve section (Chap. XCI) may be caused by reflexes set in 
motion in the neuromata of the nerve’s proximal end. In an analogous 
way, intense symptoms may be produced by the constant irritation of 
posterior roots by a new growth, and manifestations may be wholly lacking 
with complete destruction of such posterior roots. 

Other authors have expressed the opinion that when nerve impulses are 
interrupted, the nutrition of tissues goes on, but with diminished activity. 
Under such conditions only special demands upon the functional activity of 
the nerves may bring deleterious changes. The tissues are believed to be¬ 
come more sensitive, so that increased pressure may lead to necrosis as in cases 
of myelitis; or, the insensitive cornea may be injured through the very slight¬ 
est external traumata with resulting ulcer formation. In many examples of 
trophic disorder, the occurrence of a trauma might be regarded as sufficient 
to explain the condition, since under normal circumstances the tissues of the 
body demonstrate their ability to resist external influences and conserve 
their nutritional integrity. Slight external irritants, when followed by trophic 
derangement, indicate a disorder in trophic innervation (trophic function). 

Whenever the skin cannot meet the exigencies of the normal external 
accidents and stresses and reacts with evident nutritive disorder, we are 
warranted in assuming that impairment of the neurotrophic function exists. 
Conditions of deranged trophoneurotic function may escape our cognizance, 
unless each set of the motivating factors resulting in manifest impairment of 
tissues be carefully analyzed and weighed. 

Most authors agree that the existence of isolated trophic nerves is not 
supported by present evidence. That the nervous system exercises a trophic 
function cannot be denied, and the trophic influences doubtlessly pass through 
paths serving other purposes. The skin receives the trophic impulses by way 
of the sensory and vasomotor paths, and may travel in a direction opposed to 
the usual impulses travelling through them. The action of reflexes by way 
of the sensory to the vasomotor paths is also of great importance in deter¬ 
mining nutritional effects. 


100 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XVI 

GENERAL CONSIDERATIONS OF THROMBOSIS 

Forms of Thrombi. —To elucidate both the pathological and clinical 
phenomena observable in cases of gangrene, a clear concept of the process 
of thrombosis is essential. The practitioner should not be satisfied with a 
loose notion regarding the pathology and causation of the thrombotic lesions 
that partly or completely occlude the arteries and veins. 

The coagulation and the loss of the fluid state of the blood, when it occurs 
during life, becomes one of the morbid processes. For the recognition of 
thrombosis as a disease, we must differentiate intra vitam and postmortem 
clots. Although the word thrombosis has been employed in a wider sense 
to include also the intravascular accumulation of living cells of varying 
types of tissue complexes and of bacteria, the presentation of this subject 
will be restricted to descriptions of agglutination , conglutination and coagula¬ 
tion of the blood elements, with the formation of clumps or solid masses of 
various types and forms. 

The intravascular solidification of the total blood in a vessel, or of any of 
the component parts in the living organism, is the result of changes in those 
factors which under physiological conditions preserve its fluid nature. 
These factors are the physical power of the blood circulation and the chemical 
constitution of the blood. The blood flow (circulation) can undergo changes 
by reason of either general or local disturbances in the blood pressure, as 
well as through alterations in the structure and capacity of the vessel wall. 
The chemical composition of the blood depends upon the intrinsic vital 
function of the blood cell as well as upon the action of the vessel wall. But 
both the mechanics and the chemistry of the blood may suffer change through 
the action of solid or fluid bodies of alien nature that penetrate into the blood. 
These considerations would lead to a differentiation into mechanical and chem¬ 
ical causes of thrombosis. It is difficult, however, to strictly separate causal 
moments. 

Authors differ as to whether all thrombi represent some form of decay (necrosis). 
According to some, thrombosis should be regarded as a form of intravascular blood necrosis, 
and that in the process following mechanical or chemical causes, there form certain materials 
made up of single or a combination of confluent blood components. 

The word thrombosis signifies plug formation within the blood vessel, 
leading to partial or complete closure of the vessel lumen. 

Various conditions lead to thrombosis. The following types have been 
described: (i) coagulation with separation of a solid fibrous (fibrinous) sub¬ 
stance (clotting); (2) an aggregation of various morphologic constituents 
or agglutination ; (3) the separation and cohesion of certain elements, called 
conglutination. The healing and degeneration of these elements in the latter 
process has also been called congelation. 

The determining factor in thrombus formation seems to be the aggregation 
of elements. This may be brought about through the influence of the vessels 
themselves (injury of the vessel wall), through the action of the blood ele¬ 
ments, or through agencies altering the blood elements, through hemolysis, 
precipitation, agglutination or destruction. Coagulation or clotting then 
follows as a secondary phase, and is rarely primary. 


GENERAL CONSIDERATIONS OF THROMBOSIS 


101 


The distinction has also been made between pure conglutination throm¬ 
bosis, in which the separation and aggregation of elements is essential and 
determining, and a combined thrombosis, of the clotting type, called coagu¬ 
lation thrombosis. 

Thrombi form because of impairment of the blood stream, injury of the 
vessel wall, or changes in the blood composition. 

Types of Thrombi.— White thrombi may develop in flowing blood from the 
heaping up of platelets or leukocytes, or both, with or without fibrin forma¬ 
tion. When, with the blood at a standstill, the red blood cells participate 
particularly, a red thrombus usually combined with a white one (mixed throm¬ 
bus) is formed. Such segregation of blood platelets from leukocytes can 
result from mechanical factors or chemotactic influences. Of the mechan¬ 
ical factors, centrifugal dispersion or confluence in wave nodes may be 
mentioned; chemotactic forces cause the attraction of leukocytes into platelet 
centers, as the result of chemical changes in the vessel wall. When the ele¬ 
ments that participate undergo death, they form a coherent, colorless mass that 
offers resistance to the blood flow, and simultaneously delivers a ferment 
necessary for the coagulation of the fibrinogen of the plasma. 

White thrombi can be made up of pure platelets, but only so when they are recently 
produced; or, where by reason of the strength of the stream, deposition of leukocytes and 
fibrin is prevented. This occurs in the aorta over atherosclerotic patches. Usually white 
thrombi are made up of platelets and leukocytes, the leukocytes being attached to a ground¬ 
work of fused platelets. Fibrin and red blood cells are admixed. When white blood 
corpuscles preponderate, then we speak of a leukocyte thrombus, but platelets are always 
present. The white thrombus is the typical segregation (Abscheidungs Thrombus). 
It is formed when the vessel wall is injured, without added circulatory disturbances; or it 
can constitute the essential structure of mixed thrombi. 

Red thrombi occur either when there is rapid coagulation, or when the 
stream is markedly arrested or retarded, usually over a deposit of white throm¬ 
bus in a retraded stream. In the red thrombus there is a rich network of 
fibrin with enmeshed red and white blood cells, which are not equally dis¬ 
tributed. The red thrombus is particularly a coagulation thrombus and its 
loose structure permits of the tearing off and the transportation of fragments. 

Mixed thrombi form the greatest percentage of all. They are made up of 
red and white portions (with head and tail, Aschoff). 

Hyaline thrombi are found in small veins and capillaries as complete 
homogenic bodies, or diffusely filling the lumina. They are made up either 
of fibrin plugs or of a homogeneous mass of platelets and leukocytes. Toxic 
substances such as serpent venom, ferments, the products of the influence of 
cold and heat, mushroom poisoning, and the toxins of eclampsia, infectious 
diseases, (diphtheria, pneumonia, scarlet fever) have been known to pro¬ 
duce these plugs. They are not so apt to occur in the extremities; more 
usually are they observed in the kidneys, intestines, lungs and brains. 

Blockage of the small vessels may be produced by the spodogenic thrombi , 
where precipitates and destroyed fragments of blood corpuscles fill the lum¬ 
ina. Poisons such as lead, anilin and the absorption from burns, are the 
causes. A similar condition is produced through sudden hemolysis and after 
blood transfusion, when so-called shadows of blood cells (thrombi) or plate¬ 
lets and leukocytes fill the vessels. 


102 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XVII 

THE FORCES ENGAGED IN THROMBUS FORMATION 

Coagulation and Agglutination—These must be differentiated. They 
will be described as they occur outside of the vessels, and then as they appear 
in the cadaver. 

Extravascular Coagulation.—Microscopic observations of the first changes in a fresh 
clot, o*f blood (hanging drop) kept in a moist chamber, may be summarized as follows: The 
platelets agglutinate and accumulate in small heaps, in which the contour of the individual 
platelets shows dissolution of their peripheral margins. The platelets stick together and 
to the glass chamber. The agglutination of the red blood cells into the coinstack form 
takes place simultaneously, and the rolls sink gradually to the lowest part of the drop. 
Later they fuse to such an extent that they form solid bodies simulating hyalin thrombi. 
Shortly after the process of agglutination, the deposition of the fibrin elements takes place. 
This probably depends upon the breaking-down of the platelets. At the inception of the 
process, the ultra microscope shows fine linear crystal-like threads which grow under the 
eye of the observer, and increase in number. The fibrin masses in the hanging drop usually 
show at the very beginning a relationship to the platelets radiating from these. Then the 
crystalline form becomes lost and the fibrin attains the appearance of threads, thicker in 
the center than in the rest of their course. 

In sterile tubes, if coagulation is rapid, the red blood cells may be thrown out at different 
levels, giving the clot a variegated appearance. If agglutination and gravitation are 
absent, the blood may solidify into a homogenous red column. The process of coagulation 
begins at the periphery and advances towards the center. Later the coagulum contracts 
with the expression of clear serum. This filtration takes place through a dense fibrin 
reticulum that allows neither red nor white blood cells to penetrate. 

In the cadaver, coagulation of stagnant blood is modified through the continuance of 
a certain degree of inhibiting action of the inner vascular walls. Its process is slower and 
incomplete as compared with extravascular coagulation. Even if an abnormal amount of 
ferment is present in the capillaries and small vessels (as in pneumonia) coagulation does 
not take place. Inhibitory influences exerted through the vessel wall are held accountable. 

Whilst coagulation incited by a foreign body takes place away from the periphery (as 
in the glass tube), early clotting in the cadaver is seen in the central portion of the blood 
column, the clot being separated by a layer of fluid from the vessel wall. The inhibitory 
process is believed to be due to injury, and deterioration of fibrinogen and fibrin ferments. 

Between the one extreme of fluid blood, and that of delayed coagulation (cadaver) with 
its homogenous red clot, there are manifold mixtures of a bacon-like clot (speckgerinnsel) 1 
with the red masses or cruor. The mixtures vary in that bizarre layers, combination clots> 
islands, inclusions or white clots are enclosed in the red portion. Evidently in the cadaver 
the coagulation takes place more slowly, at varying rates and at different points. 

The red post-mortem clots (cruor masses) have the general appearance of the clot in 
vitro. Microscopically there is very slight platelet agglutination. The more dense the 
coagulation, the denser the fibrin net work, and the more complete is the absence of the 
fibrin centers. In the post-mortem clot the fibrin is exhibited throughout and shows dis¬ 
tinct platelet centers. In rapid coagulation, there is probably a sudden invasion or satura¬ 
tion of the blood with fibrin ferments. This is artificially producible through the injection 
of tissue juices. The fibrinous network may then become so dense, that its interstices are 
smaller than the red blood cells. As a result, mechanical breaking-up of the cells may 
ensue when the fibrin mass contracts. Where there is slow coagulation as in the bacon-like 
clot (post-mortem), the absence of erythrocytes with the coarse platelet centers 
is noteworthy. 

The Process of Agglutination .—The agglutination of the platelet is the 
signal for the rapid excretion of fibrin. So also blood whose red cells have a 
special tendency to agglutinate, is apt to clot rapidly, although no morpholog¬ 
ical relationship between fibrin formation and the agglutinating red blood 
cells is demonstrable. Substances that inhibit agglutination also diminish 

1 A term given to post-mortem clots in which the red blood cells have fully gravitated. 


THE FORCES ENGAGED IN THROMBUS FORMATION 


103 


fibrin coagulation. However, the two processes of agglutination and fibrin 
clotting cannot be regarded as identical, since either can occur independently. 

Agglutination of platelets, and less frequently of erythrocytes occurs; it is absent 
altogether in the case of leukocytes. 

Agglutination represents a disturbance in the normal repulsion between corpuscular 
elements on the one hand, and the surrounding plasma on the other. Spatial conditions 
even with chemical integrity of the elements, may play a role in the production of agglutina¬ 
tion. Thus, when, by virtue of mechanical conditions the cellular elements are approxi¬ 
mated, the quantity of the inhibiting fluid between them may not suffice to prevent a 
tendency to cohesion. It is this mechanical relationship that may be a factor in the 
production of thrombi of mechanical etiology; and it throws light upon the importance of 
movement in the fluid, for the conservation of the blood. 

If we believe that agglutination occurs by reason of dissolution of very delicate surface 
coverings about the erythrocytes or platelets, we must also accept the view that the 
microscopic cell limitation is only the boundary of the solids, but not of the fluid constit¬ 
uents. . According to Beneke, when no cohesion of cells occurs, any normal process of 
attraction that may exist is inhibited by the opposing forces in the surrounding plasma. 
Two forces are apparently necessary for agglutination, firstly the specific function of the 
corporal elements, and a contrary force emanating from the blood plasma. From the 
corpuscles, streams of fluid matter are supposed to emanate. The production of a cohesive 
surface substance can be increased. Foreign bodies are known to have such influence on the 
platelets, and overproduction of adherent or cohesive substances resulting, implicating more 
and more new platelets, and attracting these to the incipient conglomerates. Chemical 
injury of the platelets leads to overproduction of this surface substance, or to destruction 
of platelets even without contact of a foreign body. 

Fibrin Coagulation .—This is a complicated process in which a fibrous 
substance, called fibrin, separates out from the plasma in the form of a reticu¬ 
lar mass, and unites the corporal elements of the blood into a solid mass. 

In the blood plasma there are fibrinogen, thrombogen and calcium salts. Thrombogen 
is the incomplete antecedent of the ferments, and is converted by the activating substance 
thrombokinase into the effective coagulating ferment thrombin. This can occur, however, 
only in the presence of the calcium salts. This thrombokinase originates mostly out of the 
blood platelets which agglomerate at the incipiency of the clotting process, break down and 
form the center of radiating fibrin formation. Possibly leukocytes also participate in this 
action. Ordinarily for the creation of thrombokinase out of platelets or leukocytes, the 
latter must leave the vascular channel, and in this case some of this kinase is also delivered 
from the salt of the wound surface. Through the action of thrombin (derived from throm¬ 
bokinase, plus thrombogen) upon fibrinogen, the latter is broken down into fibrinoglobulin 
and fibrin. 

In the vessels themselves the intact endothelium of the intima is supposed to inhibit 
clotting, partly in that the smooth surface exerts no irritation upon the elements that 
deliver kinase, and partly in that it forms an anti-clotting, inhibiting substance 
antithrombin. 

More recently the following views have been expressed regarding coagula¬ 
tion (Bordet 1 ). The two so-called mother substances active in coagulation 
are cytozym—a lipoid derived from the tissue cells and blood cells; and sero- 
zym present in the serum These are the precursors or mother substances of 
thrombin and prothrombin. 

Serozym is easily destroyed by heat; whereas cytozym, the active princi¬ 
ple of platelets resists evemoo 0 C. without losing its properties. The latter 
also exhibits in extract the characteristics of lipoids, especially lecithin. 

Bordet believes that cytozym and serozym unite in a manner similar to 
the union of toxins and antitoxins, not from true chemical affinities, but from 
contact or molecular adhesion. Serozym found in the serum is not there in 
the same condition as in plasma. It is incapable of reacting at once with 
cytozym in plasma. In other words, plasma contains a proserozym instead 
of the active serozym, so that one of the first phenomena of the whole process 

1 Bordet, Harvey Lectures, Oct., 1920, p. 36 (Lippincott). 


104 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


of coagulation would be the conversion of proserozym into a body capable of 
uniting with cytozym. 

In short, the process of coagulation may be thus summarized: Plasma 
contains fibrinogen and proserozym, the latter being converted into serozym 
by means of calcium and contact along the wall. The platelets deliver 
cytozym, which is liberated by means of contact adhesion along the vessel 
wall. Through a union of proserozym and cytozym (the former converted 
previously into serozym) thrombin is formed; and this, with the fibrin derived 
from fibrinogen, brings about coagulation. 

Scheme of Coagulation (Bordet) 

_ Plasma _ _ Cells (platelets) _ , 

Fibrinogen Proserozym converted Cytozym liberated byj 

into serozym by means means of contact (ad-l 
of calcium and contact hesion of the cells 
along the wall. along the wall). 


Union of serozym and cytozym 

J, 

-> <-Thrombin (along the wall) 

Fibrin 

contact and calcium no more necessary). 

The degenerative susceptibilities of the blood platelets towards certain 
insults and their consequent tendency to clotting, are matters that become 
easily comprehensible. 

The importance of the platelets in clotting can be studied by noting the character of 
radiating fibrin formation (fibrin stars). Such irradiation centers formed by the fibrin 
and emanating from the blood platelets are now well recognized. They are no longer 
suspected as being merely the consequence of fortuitous inclusion of platelets in the fibrin¬ 
ous network. 

However, close relationship between clotting and platelet fibrin formation cannot be 
altogether limited to these bodies. For example, leukocytes and other cells (endothelial, 
Zenker 1 ) can embody fibrin forming forces. The grouping of fibrin about such cells in 
inflammatory foci speaks for this assumption. But a special condition of the tissue 
fluids and cells is necessary to evoke the development of their coagulins, or to activate these. 

Both the quantity of ferment and the circulatory conditions play a clear r 61 e in the 
clotting process. Kiister 2 was able to show that the clot could be modified artificially 
according to the amount of fibrin ferment added, the delicate ones corresponding to smaller 
quantities, the coarser clots to the use of larger quantities of ferment. The dilution of 
ferment through the circulation is, therefore, of importance in intravascular clotting. 
In ordinary life and under normal conditions (in which the ferment is probably present 
only in small quantities) the circulation is active in producing a dilution up to a point where 
the ferment is impotent. 

Fibrin formation occurs in two varieties, in a reticular type of clotting, and in the form 
of true crystallization. Since authors differ as to the exact nature of the processes and 
division into such categories, it must be admitted that the exact limitations of crystalline 
and amorphous forms are not always possible. 

Fibrinolysis is believed to be a normal attribute of certain cells, since a fibrin network 
may disappear. The breaking down of fibrin occurs more rapidly in the cadaver than in 
vivo. Just what particular kind of ferment is at work, whether it is a proteolytic ferment 
of the leukocytes, or endothelial cells is not known. 

Antithrombin which inhibits clotting, is a constant product of the vascular wall, and 
may be regarded as a sort of vital reaction opposed to the chemical influence of the blood. 
Blood collected from organs containing numerous capillaries and relatively slow circulation, 
when taken from the living or the cadaver, has a tendency to remain fluid. Some authors 
claim to have found antithrombin hi the liver after washing the latter and after transfusing 
this organ with arterial blood, anticoagulating properties then appeared in the transfusate 

1 Zenker, Ziegler’s Beitr, XVII, 1895. 

2 Kiister, Miinchen. med. Wchnsch., 1911, No. 46. 










PHYSICAL EXPLANATIONS OF THROMBOSIS 


105 


Lipoid substances, or according to others, phosphatid substances containing C. N. and P. 
are said to be responsible for the diminished coagulating powers. An observation of no 
mean importance is the relative lack of clotting in the capillaries. 

Source and Quantity of Fibrinogen .—This does not seem to be produced by the blood 
corpuscles, since in defibrinated blood no new fibrinogen is elaborated upon standing. In 
an animal that has been thoroughly bled and transfused with defibrinated blood, the fibrin¬ 
ogen formation may attain or exceed the normal (Dostre & Mathews). Simultaneously 
the blood platelets also make their appearance, so that the fibrinogen has been considered 
as arising either from the vessel wall, or from the platelets. The latter is unlikely, since"the 
lymph may contain fibrinogen without platelets. Therefore, the excretion and quantitative 
control of fibrinogen in the blood and lymph seems to be a specific function of the tissuejcells. 
The kinase or coagulin production is a function of the living tissues, particularly of the 
platelets and leukocytes. Other cells, such as connective tissue cells, may participate. 

Congelation. —In addition to cell agglutination and fibrin coagulation 
there is another type of phenomenon which is often associated with thrombosis, 
namely, the hyaline conversion of albuminous bodies of various forms. This 
phenomenon has been called congelation as a substitute for other terms—- 
hyaline degeneration, and coagulation necrosis. This process, however, 
occurs only in dead material, even though this material forms but a part of 
the respective cell or intracellular substance (intracellular hyaline degenera¬ 
tion). Nor does it occur in every form of necrosis. The conditions for its 
development are more favorable in the living organism than in the cadaver. 
The exact nature of the process is not well known, some believing that a 
proteolytic ferment is at work. 


CHAPTER XVIII 

PHYSICAL EXPLANATIONS OF THROMBOSIS 

For a comprehension of the causation of gangrene of the extremities, it is 
well to be acquainted with the present status of the question of thrombosis. 
Much discussion has arisen since the time of Virchow as to the importance 
of the infectious or mechanical factors in the production of thrombosis. In 
his day the mechanical effects of slowing of the blood stream was regarded as 
the all important factor. The tendency of late has been to stress infection 
as the deciding factor. 

According to Aschoff 1 the concept of thrombosis can be clarified by a 
study of other physical processes with certain similarities. 

The Appearance of Thrombi.—From the pathological point of view a 
thrombus is any obstructing intravascular mass that arises intra vitam. 
Thus we can differentiate blood thrombi , tumor , thrombi and parenchymatous 
thrombi. We are merely interested here in the blood thrombi. 

These latter are characterized by their distinct stratification, by their 
friability and undulatory nature of their surface; and, are differentiated from 
post-mortem thrombi by organized adhesions to the vessel wall. 

In a well developed thrombus parts differing in color are recognized. The 
proximal portion or head portion is usually pale or a white thrombus. Adja¬ 
cent to this, the neck portion is mixed in color, and the peripheral part is 
dark red. The head may be very small, whilst the tail often measures many 
centimeters. Such are their usual appearances in the venous system. The 
red thrombi are only found where the white portion obturates the vessel. 

1 Aschoff- Beitr. z. Thombosefrage, Leipzig, 1912. 



106 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

The red portion may be absent in parietal thrombi, the white portion 
occasionally growing to considerable length in a continuing circulation. 
The white portion is the essential part of an autochthonus thrombus, and is 
the real causal factor in the whole process, whilst the red portion is only acci¬ 
dental. A pure red thrombus without a head portion is a rare exception. 
Such is the description given by Aschoff for the ordinary thrombus. That 
these rules do not obtain in inflammatory thrombi, such as are seen 
in thrombo-angiitis obliterans, will be learned in the section on that affection. 

Macroscopic and Microscopic Appearances of the Caput. Certain characteristic appear¬ 
ances of the surface of an autochthonus thrombus correspond to the internal structure, and 
have lead Aschoff to propose certain explanations of the method of its origin. The fluted 
or reef-like markings, and the reticular and streak-like shadings seen in the caput and neck 
portion of the thrombus are considered characteristic. An explanation of these markings 
is offered by this author that should lead to a correct concept of the origin of this type. 

A longitudinal section through the head and neck portion of the thrombus, shows that 
the above described superficial reef-like elevations are but the summits of beams or skeleton 
structures. These are coralliform or frame-like joistings, that form the supporting struc¬ 
tures of the whole thrombus mass. This framework is constituted by the heaping up of 
blood platelets in a fine granular mass. Above these beams or girders a fine layer of 
leukocytes is disposed, whilst in the interstices between the main support, the red blood 
cells fill out the structure. . . . . . ^ , , 

The beams themselves are disposed to each other in a regular fashion, separated by 
interspaces of varied size, and with fine branches passing upwards and downwards. . As we 
approach the caput, the blood-filled interspaces become narrower, until the supports fuse 
together into the white summits of the thrombus. 

The fibrin is almost absent in this whole structure. When it is present, it is found at the 
margin where the platelet structure is in contact with the red blood. 

When it was shown (Deetjen 1 ) that the blood platelets are independent. elements 
assisting in the circulating blood, it became comprehensible, that only in flowing blood 
could such masses of blood platelets be deposited, as are to be found in the above described 
framework of thrombi. The platelets do not originate from white or red blood cells, 
but are independent elements arising from the giant cells of the bone marrow and in the 
spleen. The platelets show a finely granular center, and a clear peripheral zone. They 
are detached from the giant cells, megakaryocytes and attain spontaneous mobility. 
These megakaryocytes of the bone marrow have been seen to interpose pseudopods into the 
capillary blood channels, and in this way the transference of the blood platelets into the 
circulation comes to pass. 

It has been shown that when a section of vessel is tied off by ligation no platelet forma¬ 
tion could be observed even after the employment of caustic irritation, whilst a typical 
platelet thrombus develops under such conditions in a vessel in which the blood circulates. 
A platelet thrombus, therefore, is regarded as arising in flowing or circulating blood. 

Formation of the Thrombus.—The framework of this type of thrombus 
is composed of a lamellar system (Fig. 41) with the elements more or less 
parallel, either transversely or obliquely disposed to the long axis of the 
vessel. In this sense, the structure resembles the effect of the ebbing tide 
on the fine sand of the ocean beach. A similar step-like line formation is 
produced by the flowing blood, the platelet masses forming the delicate 
lamellar system. Just as in slowly running water, finely divided elements 
may be deposited in a regular way so as to form reef-like formations, so in the 
blood vessel, platelets are deposited in the above-described framework. As the 
blood continues to flow, more and more platelets are attached, and further 
elaborate the structure. In the oldest portion of the platelet system, the 
renewed deposits are greatest, and finally the time arrives when the inter¬ 
stices of the lamellar system (in the oldest portion of the thrombus) become so 
minute that the blood stream becomes slower and slower, and finally ceases. 
At this moment the primary thrombus formation has attained its finality, 

1 Deetjen, Ztschr. f. physiol. Chem., Bd. 65, 1909. 


PHYSICAL EXPLANATIONS OF THROMBOSIS 107 

since no more platelet masses are added and its primary growth can continue 
no further. 

The leukocytes in this system follow the usual laws according to which the 
specifically lighter white blood cells take the peripheral zone of the stream. 
Here, since the stream is divided into numerous sub-streams by the regular 
structure, the leukocytes follow the same law and are deposited along the 
walls of the structure. 

This is the manner of formation of the head portion of the typical thrombus 
(Aschoff 1 ). 

The tail portion of the thrombus in which a platelet lamellar system is 
absent, forms in the non-flowing blood. In microscopic structure this throm¬ 
bus resembles a post-mortem clot, being made of an irregular admixture of 
red and white blood cells, blood platelets and fibrin. 

The Cause of the Development of a Platelet Thrombus.—If we compare 
the blood stream to a river in which foreign particles are distributed, the con¬ 
clusion would be warranted that any local heaping up of particles can only 
take place under an optimum special rate of flow. And so, in the blood 
stream we must presuppose that a certain diminution in the rapidity of the 
flow must take place to furnish the optimum condition. Thus in the stream 
in which barriers or dams are erected and changes in rate of flow are produced, 
deposits have been observed. So therefore, we would expect that in the 
formation of autochthonus thrombi we should find certain alterations in the 
blood stream that bring about sudden flowing or refluxes, or vortices. 

The causal factors in this type of thrombosis have been given as, 

A. Changes in the rapidity of the blood stream; 

B. Changes in the qualitative and quantitative state of the blood platelets; 

C. Changes in the inner walls of the vessels. 

A. Changes in the Rapidity of the Blood Stream .—The predilection of the venous system 
to thrombosis is in keeping with the possibilities of impediments to the normal rapidity 
of flow in them. In the venous system there are indeed sites of predilection, namely, the 
veins of the leg, the proximal portion of the femoral vein, the pelvic veins, the veins of the 
meninges, etc. Four factors contribute to the localization of venous thrombosis; (i) 
the continuous pressure on the venous wall—as is exemplified by the constant pressure of the 
column of blood in the veins of the lower extremities in the upright posture (or the action 
of intra-abdominal pressure in causing dilatation of the veins); (2) the ampullary dilatation 
of veins in the valvular pockets; (3) the possibility of reflux in the stream, first occurring in 
the proximal valves of the femoral veins; and (4) the resistance to flow that Poupart’s 
ligament offers to the current of the femoral veins in the recumbent posture. The position 
of the patient is not unimportant in determining thrombosis in veins, for an extremity that 
is constantly held under another one is more apt to show complicating thrombosis. The 
compression of the left iliac vein through the iliac artery is not to be disregarded in its effect 
in impeding flow in the veins and leading to left-sided crural thrombosis. 

B. Changes in the Platelets .—Whilst retardation of the flow is an important factor in the 
production of thrombi, the accumulation of platelets may be influenced otherwise. These 
thrombi have been variously called separation or accumulation thrombi (Abscheidung und 
Anhaufung). These terms have been applied because of the fact that the platelets are 
more or less intimately agglutinated. And so, in the literature, we find besides the 
appellation “ accumulation ,” also the words “conglutination” and “ agglutination ” descrip¬ 
tively used in this connection. Here we presuppose an alteration in the viscosity of the 
platelets. We do not know, however, whether increased coagulability of the plasma also 
determines a more rapid agglutination of the platelets. Variations in the fibrinogen 
content may have some influence. Increase in the fibrinogen content alone per se does not 
lead to thrombosis, so that a direct causal relationship cannot be accepted in the present 
state of our knowledge. 

Certain it is, that in artificial anemia, the platelets become markedly increased in 
number, and from this we may draw as a corollary the noteworthy observation that persons 

1 Aschoff, Loc. cit. 


108 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

rendered anaemic by operation or gynecologic or obstetrical conditions show an increased 
tendency to thrombus formation. . . 

C. Changes in the Vessel Wall— The role of alterations of the mtima in the production 
of thrombosis has been much overestimated. It is a well-known fact that the atherosclerotic 
aorta, and other large arteries in spite of very intensive intimal changes , may he free of all 
thrombus formation. It has been asked as to whether thrombosis can only occur when the 
intima has been damaged; chronic changes in the intima of the vein alone do not play 
a determining role in causing thrombosis. Where, however, there is advanced phleboscler- 
osis with rigidity of the vein walls and valves, with consequent circulatory impairment, 
we may conclude that a causal relationship exists. When, however, the intima is suddenly 
robbed of its endothelium covering, a pathological reaction of the tissues is necessarily 
unavoidable. In such a case it is the alteration in the territory of the wound that causes 
the thrombosis. 

Coagulation in the Process of Thrombosis.—The observation (Baum- 
garten) to the effect that fluid blood does not clot in a section of a vessel 
that has been ligated in two places, would at first sight offer insurmountable 
difficulties to any explanations of the clotting process. 

Aschoff says that the breaking down of platelets sets free fibrin ferments 
that admix with the surrounding plasma, and by a process of diffusion pass in 
a peripheral direction where the effects can be manifested. In the origin, 
therefore, of red thrombi , we presuppose not the separation of corporal ele¬ 
ments of the blood (as in the platelet thrombi), but notably the throwing out 
of fibrin (as in the ordinary clotting process). And so the red clot (coagula¬ 
tion thrombus) is to be differentiated from the platelet (segregation or conglu¬ 
tination) thrombus. Some authors distinguish between conglutination or 
agglutination, and accumulation thrombosis and coagulation thrombosis. 
Whilst in the segregation (conglutination) type of thrombosis, the slowing of 
the blood stream and the quantitative and qualitative conditions of the plate¬ 
lets and their viscosity are the essential factors, so, in the case of the coagula¬ 
tion (red) thrombosis, the cessation of the stream and the ferment elaboration 
are essential. 

It is evident, then, that one type of thrombus (the platelet thrombus) 
leads directly to the other type, the coagulation thrombus. Similarly we see 
in thrombo-angiitis obliterans a specific type of clot doubtlessly of inflam¬ 
matory nature, directly associated with a coagulation clot that caps the 
terminal portion of the former (Chap. LXI). 

Primary Coagulation Thrombosis.—It is a difficult matter to produce a 
primary coagulation thrombosis experimentally. Cessation of the blood 
flow alone does not suffice when the ferment development is not adequate. 
Indeed, optimum conditions, with a proper relationship between rapidity of 
flow and quantity of ferment are necessary to bring about the result. For, if 
ferment is present in large enough quantities, even the flowing blood may clot. 

In some of the experimentally produced clots we may be dealing either with fibrin 
coagulation or what is known as “precipitation thrombosis.” Two other factors, however, 
are known to bring about coagulation thrombosis. These are ligation and infection. 

When the fibrin ferment that originates in an injured vessel wall through 
ligation can adequately exert its influence on the continuous non-flowing 
blood column, coagulation thrombosis may occur. The platelet thrombosis 
may also develop where the dead portion of the vessel is in contact with the 
blood stream. Both forms of thrombosis are possible, whilst with very slight 
injury to the wall neither one of these may follow. 

In the so-called infectious type of thrombosis, the thrombus formation may 
precede the infection or be caused by the infection. In the puerperal throm¬ 
bosis, and in post-operative infectious thrombus formation, by virtue of the 


PHYSICAL EXPLANATIONS OF THROMBOSIS 


109 


liberation of fibrin ferment, coagulation thrombosis may occur in numerous 
veins, and where the blood flow is interfered with, the platelet thrombosis 
may develop. If infection (particularly streptococci) be superadded, an 
inflammatory reaction within the vessel wall with the migration of leukocytic 
elements from the periphery into the vein wall, is to be expected. Puerperal 
cases often evidence a puriform condition within the veins, with marked 
periphlebitis, the picture simulating abscess rather than infectious throm¬ 
bosis. In such cases the infection travels through the vascular walls rather 
than by way of their lumina. 

The thrombosis that occurs in direct association with an inflammatory area is a compli¬ 
cated process. At first the venous tributaries become the seat of thrombosis, probably of 
the coagulation type, by virtue of the liberation of the fibrin ferment in the inflammatory 
toxic process. Then secondary invasion of bacteria takes place, and finally the larger veins, 
by reason of interference of the circulation, become the seat of platelet thrombosis. It is 
difficult to differentiate accurately in all cases between thrombosis as the result of an infec¬ 
tion, or a thrombus secondarily infected. 

Metastatic (?) or Distant Thrombosis .—It is possible to explain distant thromboses in 
three ways: (i) the microorganisms in the blood cause a local change in the wall of the 
vessel with secondary thrombosis; or (2) that in some unknown way, coagulation phenom¬ 
ena are brought about in the blood by the organism; and (3) that the primary thrombosis is 
independent of the infection, the manifestations of thrombophlebitis being produced by 
secondary invasion of the clots with the organisms. 

(1) Metastatic inflammatory changes in the wall are clinically rare, but may possibly 
explain the occurrence of tubercular and syphilitic thrombophlebitides. 

(2) Direct coagulation through the action of the circulating organism is only a hypo¬ 
thetical explanation, since experimentally such action of bacteria could only be produced 
when stasis in the blood stream is an added factor. 

(3) Primary thrombosis with secondary infection is the most common type. In the 
femoral vein where thromboses so frequently occur in post-operative cases, the thrombosis 
according to Aschoff, was found to be of the platelet type. Distant thrombosis in the iliac 
veins occurs with no direct connection between the site of operation and the site of the 
thrombosis. Here, too, platelet thrombosis is the rule and when infectious thrombi are 
found, these show the bacteria in the platelet masses. The thrombosis, therefore, just as 
in the non-infected cases is the result of local alterations in the stream, and not the imme¬ 
diate result of infection, the bacteria invading secondarily. Then, as the bacteria multiply, 
degeneration of the thrombus elements takes place, and infiltration of the vessel wall with 
leukocytes follows. Superadded to such a thrombus there may be a secondary thrombosis 
extending centrally. 

Thrombosis in Thrombo-angiitis Obliterans.—How are we to explain 
this variety of thrombosis, one that is exquisitely of the red variety, but in 
which three different forms are in evidence? The pathology of this form will 
be described in detail elsewhere. Here, for clarity it may be well to 
anticipate by stating that a red (or mixed) form is the immediate sequence 
of lesions in arteries and veins, whose walls have become the seat of an 
acute inflammatory process. Stasis probably plays a role, for only 'n this 
way can we explain the predilection of the vessels of the lower extremities 
for this disease. Secondary changes occur in the clot by the transmigra¬ 
tion of corpuscular elements through the walls of the vessels. A “specific” 
architectural picture is thus evolved that seems in the light of our present 
knowledge to be pathognomonic. The latter changes are reactive, resorptive, 
and (teleologically speaking) paradoxically curative and baneful in nature. 

The characteristic form of clotting could, in the interpretive system of 
Aschoff, be regarded as of the type due to “ metastatic inflammatory changes 
in the vessel walls,” although a specific organism has eluded the search of 
investigators. So also, could the process be included in the above-mentioned 
third category. For, the inflammatory and abscess-like foci in the clot 
might be regarded as indicative of secondary infection. 


110 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


A bland, red form of thrombus within normal vessel walls, and evidencing 
no inflammatory and none of the specific reactive and resorptive phenomena 
is often found as a sort of cap surmounting the typical variety (accretion or 
stagnation thrombus). This, it would seem, is due to local cessation ot t e 
stream, possibly aided by the liberation of fibrin ferments. 

The third form includes only the intermediate and final products ol the 

first type. 

Precipitation Thrombosis.—This is another form of thrombosis that has a rather 
theoretical than experimental interest. It may be described as that form in which thrombi 
result from the action of chemicals precipitating albumin. Whenever mucous membrane is 
cauterized chemically, such thrombi develop in the smallest veins; so also, when a heterolog¬ 
ous serum or a specific precipitating serum is introduced into the veins. This phenomenon 
belongs to the type known as agglutination, the agglutinating red blood cells playing an 
important role. In the thrombi resulting from the action of poisons (ncin, adrin, snake 
venom), the clotting is partly due to agglutination phenomena, and partly to the obstruc¬ 
tion of the smallest vessel with broken-down red blood cells. The effect of burns is a similar 
one. Aschoff has designated the type with breaking down of red blood cells as spodogemc 
• thrombosis. 


Classification of the Thrombotic Process 1 


According to form 


According to causal genesis 



i. Seggregation (separation or 
conglutination thrombo¬ 
sis) . 


2. Coagulation thrombosis 
(clotting). 


3. Clumping thrombosis (ery¬ 

throcytic agglutination). 

4. Precipitation thrombosis. 


5. Spodogenic thrombosis. 


Local retardation of the 
stream. 

Quantitative and qualita¬ 
tive alterations in the 
platelet. 


Local cessation 
the stream. 
Fibrin ferment. 


of the 


Agglutination of the red 
blood cells through blood 
poisons. 

Albumin precipitation 
through caustic chemi¬ 
cals. 

Breaking down of red cor¬ 
puscles through blood 
poisons. 


(a) Physiological narrowing or dilata¬ 
tion. .phys. dilatation thrombosis. 

(b) Dilatation with pathological changes 

in the walls .pathological dilatation 

(c) Static factors.static thrombosis 

( d ) Compression, .compression thrombo¬ 

sis. 

(e) Vessel injury. . traumatic thrombosis. 

(f) General weakness of the vascular 

system.marantic thrombosis. 

(g) Alterations in the blood. 

blood deterioration thrombosis. 

( h ) Inflammatory wall changes. 

inflammatory thrombosis. 

Ligation ■> 

Placentar [ Stagnation thrombosis, 

detachment J 

Inflammation. Inflammatory thrombosis. 


.Toxic thrombosis. 


1 Aschoff, L, Beitr. z. Thrombosefrage, Leipzig, 1912. 


Ribbert 1 differs in his conception of thrombosis from the views above expressed in that 
he believes that the platelet structure is a secondary formation after platelets have become 
adherent to an injured intima. When there is a small circumscribed lesion of the intima 


1 Ribbert, Virchow’s Arch., 220, 1915, p. 133-147. 



























MECHANICAL TYPES OF THROMBOSIS 


111 


(experimentally produced) a small rounded mound of platelets covering the area is noted. 
An intimate relationship is always seen between the injured area and the platelet deposit. 
According to his view a retardation of the blood current, although it favors the adhesion of 
platelets, is not the determining factor, but the very beginnings of platelet deposit permit of 
continued deposition including also leukocytes and fibrin. In this way lamellae perpen¬ 
dicular to the blood stream originate. Where there is a “system” of platelet framework, 
Ribbert presupposes the existence of numerous platelet mounds, each giving rise to its 
platelet beam. 


CHAPTER XIX 

MECHANICAL TYPES OF THROMBOSIS 

For a better understanding of the origin of thrombi within the body, a 
brief resume of results of experimental work and of observation on effects 
of intravascular physical phenomena may elucidate the subject. In the 
following exposition the work of Beneke, 1 Lubarsch, Zahn and others has 
been extensively drawn up. 

The deleterious influences can set in acutely or slowly, or may take the 
form of a variation in the character of the stream of flow. The former of these 
constitutes stagnation thrombosis, the latter the pulsion 2 thrombosis. The 
former of these corresponds to a certain extent to the coagulation type of 
of thrombosis, the latter with the accumulation or seggregation type. 

Stagnation Type of Thrombosis.—Experimentally, it has been shown that blood con¬ 
tained between two ligatures in a living vessel with uninjured vessel walls, will remain fluid. 
But such a section of vessel when cut out of the body and exposed to ferments, or when 
tissue extracts are injected (coagulins), undergoes early coagulation. In such stagnant 
blood, coagulation does not take place until by virtue of marked injury of the vessel wall at 
the site of ligation, or through chemical lesion of the wall and thermic influence, localized 
special causal moments have become established. 

In territories undergoing stasis, increasing degeneration of the vessel wall is believed to 
take place by reason of inadequate gaseous interchange, with resulting breaking-down of the 
blood corpuscles. Their hemoglobin-free detritus may then fill the lumina, or lead to 
hyalin thrombosis. Then fibrin ferment develops, resulting in coagulation in spite of the 
inhibiting influences of the vessel walls. 

In short, experiments seem to warrant the conclusion that true thrombosis results only 
then in stagnant blood when added mechanical thermic or toxic influences play a role. 

Pulsion Thrombosis.—In this group we presuppose that through special modalities of 
flow, the normal mixture or distribution of the corporal blood elements is disturbed with 
a tendency to local aggregation of special groups or types, particularly of blood platelets. 
In this way agglutination, coagulation and congelation leading to plugs or thrombus 
formation are favored. Essential for such modifications are principally an abnormally 
strong development of the plasmatic marginal stream. These currents can be observed 
in flowing blood at the vessel wall, and they form the peripheral zone in which erythrocytes 
are absent. The physiologic significance of this territory is the constant reciprocal exchange 
of chemical relations between the blood and the vessel endothelium. Through this 
exchange the plasmatic marginal current is doubtlessly influenced. The rolling motion of 
the leukocytes independent of the axial current is believed to be partly due to the osmotic 
processes that are an expression of the secretory activities of the mural vascular elements. 

For an understanding of the mechanical forces the excellent description of Beneke 
will be extensively used. 

According to general hydro-dynamic laws the forte of the axial current (in a non-living 
tube) is the strongest and diminishes in intensity towards the wall of the tube. Theoret¬ 
ically there is a thin resting layer directly against the wall. The rapidity and breadth of 
the marginal current depend upon the energy and form of the total stream. A rapidly 

1 Beneke, Krehl-Marchand Handb. d. allg. Path. 

2 Terms used by some of the Continental writers. 



112 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 34. —Schematic representation of increasing size of marginal zone with (diminution of 

pressure. ( Beneke ) 



Fig. 35. —Schematic representation—changes in marginal zone at points of local dilatation. 

( Beneke) 



Ai, 

1 \ 

Fig. 36. —Schematic representation—formation of whirls or eddies in vessels by reason of 
abrupt changes in the character of the lumen. ( Beneke ) 









MECHANICAL TYPES OF THROMBOSIS 


113 


flowing axial current develops considerable natural pressure, and the marginal current can 
become insignificant; the less the lateral pressure, the broader the slow marginal zones may 
become. 

In Fig. 34 the dark central area to the left represents a strong rapidly flowing stream 
that develops an increasingly broader marginal zone at a, where its diminishing intensity is 
also expressed by lighter shadings. 




Fig. 38.—Schematic representation—formation of whirlpool where two marginal cur¬ 
rents ( x-y) meet at a. ( Beneke) 

Local dilatation (Fig. 35 at a) and general dilatation at ( b ) are accompanied by similar 
changes in the marginal zones. 

Abrupt changes in a tube or vessel wall with generalized or local changes in diameter of 
the lumina (Fig. 36) may cause the formation of whirls or eddies or vortices. The propel¬ 
ling force of the stream current perpetuates these eddies, whilst any contained particles at 
the periphery of the eddies are cast off tangentially. 

s 







114 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Narrowings in the stream through projections from the walls cause quite different 
phenomena. In Fig. 37 it will be seen that the upper portion of the stream conserves its 
strength, whilst the lower is altered through the presence of the dam-like obstruction at a. 
Behind the dam, condensation and attenuation of the axial current are produced together 
with waves. The altitude of these waves diminishes as they recede from the obstacle, 
varying according to the strength of the axial stream, their length being related to the 
height of the obstruction. Beyond the obstacle an eddy is formed that tends to flow in a 
everse direction. 

It will be noted that just beyond the dam (to the right at a) there is a space, and 
then follows the eddy. The course of this eddy or whirlpool has been shown to be so 
great that solid particles in an experimental stream are thrown backward against the 
stream into the dead space. A correct understanding of these phenomena will enable the 
reader to properly interpret the theories of Aschoff. 



Fig. 39. —Schematic representation—the effect of ligation seen in the formation of whirl¬ 
pools at the closed vessel ends. ( Beneke ) 


Fig. 38 shows the development of a whirlpool where the two marginal currents of x and 
y meet at a. Whichever of the two streams is the stronger (let us suppose y) will displace 
the eddy into the lumen of the other, into a point of rest (<2). The stronger the pressure 
differences between the two streams, the greater the transference into the lumen of the 
weaker current. 

The effect of ligation is depicted in Fig. 39 at a, with the current running in the direction 
of the arrow. The current flows with accustomed full rapidity through the branch (*'), 
and forms a whirlpool in the blind end. A collateral (y') which leads from the distal vessel 
becomes the seat of a reverse current. In the blind end of this part of the eddy a larger 
eddy is formed. 

According to Eberth-Schimmelbusch (Fig. 40) the marginal current of the blood 
contains normally only white blood cells, whilst the platelets are admixed with red blood 
cells in the axial stream. Simple diminution of the rapidity of the current is followed by a 
distinct increase jn the parietal leukocytes. With further diminution in flow the blood 
platelets are cast into the marginal zone in increasing numbers until the latter occupy most 
of this region. Even with this phenomenon a true thrombus does not form, and with a 
change in the rapidity of the current, these corporal elements can be again withdrawn into 
the central portion of the stream. 

According to mechanical laws, the heavier red blood cells must follow the axial current, 
and according to the law of centrifugal motion must move in the periphery of the eddies. 
The marginal zone, as also the center of the eddies, must therefore under favorable cir¬ 
cumstances contain mostly leukocytes and platelets. The breadth of the marginal zone, 
as also the extent of the whirlpool centers decrease with the intensity of the lateral pressure 
in the channel. Increased pressure tends to force the corpuscular particles into the eddy, 
against the latter’s centrifugal tension. Per contra, when there is little pressure the eddy 
tends to broaden and the steadier elements can be more easily precipitated externally, and 






MECHANICAL TYPES OF THROMBOSIS 


115 


the separation of specifically lighter articles from the heavier is favored. Since the eddy 
becomes broader with diminution in rapidity of the stream, the number of platelets and 
leukocytes increases with weak current. 

Solid plugs develop experimentally with mechanical vascular lesions. When acupunc¬ 
ture is used in experimentation, all the blood corpuscles are pressed against the injured 
area, and then become converted under pressure into a hyalin stagnation thrombus. 
Where circulation is still present with waves and eddies, leukocytes and platelets coalesce. 
The latter agglutinate and form the beginnings of true thrombi. Where the current is very 
rapid, the thrombi may be absent, because the platelets are torn away soon after attach¬ 
ment. Changes in direction and weakness in the current are important factors in 
the formation of thrombi in experimentation. 

; 2 3 



Fig. 40.—(1) Normal circulation showing central axial current and plasmatic marginal 
zone with discrete leucocytes. 

(2) Circulation of diminished rapidity, the red blood cells visible in the axial current, 
accumulation of leucocytes at the parietes and beginning mural attraction of the platelets. 

(3) Markedly slow circulation, marginal accumulation of platelets and leucocytes with 
sluggish, narrowed axial current. ( Eberth-Schimmelbusch) 


It has been shown, however, that although trauma is an important predisposing factor 
in thrombus formation, pure mechanical agglutination up to complete thrombus formation 
can occur , as the result of changes in the current alone. 

In addition to the mechanical factors, chemical influences have been thought to explain 
thrombosis. Indeed, the experiments with hirudin seem to show that venous tears after 
hirudin or pepton injection are followed by typical platelet thrombosis, usually without 
fibrin, in inverse proportion to the amount of anti-coagulin injected. 

When foreign bodies are introduced into the circulation, agglutinated platelets accumu¬ 
late in thrombus-like formation over the foreign body in very few minutes. About such 
bodies, eddies and waves develop that lead to agglutination of the platelet elements. 

That chemical influences must be taken into consideration, however, is demonstrated 
by the fact that foreign bodies covered with paraffin do not show such platelet agglutination. 
Perhaps in the case of foreign bodies, just as in the traumatic thrombi, the death of isolated 
leukocytes and platelets adherent to the foreign body evokes the incipiencey of further 
agglutination and attachment of the mechanically concentrated platelet masses. Plate¬ 
lets occur in places in which the current is relatively retarded. 


































116 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In the ligated vessel , whirlpools of varying size and density are occasioned by the 
current. Usually with adequate collateral and intensive circulation thrombosis does not 
occur, since small agglutinates are easily detached by the current. In the presence of weak 
currents, however, thrombus formation occurs with growth of the latter into the free lumen 
of the vessel without contact with the walls. 

But the retardation of the stream alone after ligation of a vessel does not seem to be the 
only factor in thrombosis. It must be conceded that at the present state of our knowledge 
it has not been possible to simulate the marantic thrombi in an experimental way. Some 
other chemical constituent of the blood must be sought for, which, in. the presence of 
mechanical contributing factors suffices to bring about thrombosis. Lipoid substances are 
believed to be not unimportant in this connection. . 

Stagnation Thrombosis.—Some observations would seem to indicate that thrombosis 
does not normally occur in a stagnant flow. The fact that it is absent in the umbilical 
artery after ligation of the cord is cited as an argument against the mechanical theory; 
and also the fact that vessels in the case of atherosclerotic closure of the crural arteries do 
not necessarily become closed by thrombi. 

The instances where plugs do occur, however, in these circumstances cannot be ignored. 
Here possibly an additional factor besides the stagnation, either a change in the vessel wall 
or of the contents, is responsible. 

In the case of the capillaries and small vessels, stasis contributes a certain essential 
condition, be it through simple mechanical interference to the outflow with a continuous 
inflow, or be it through the chemical changes in the tissues and vessels that are thus engen¬ 
dered. The phenomenon of stagnation does not seem to be the only effect of retarded 
circulation. In addition to the diapedesis and capillary dilatation, the erythrocytes are 
massed together and compressed, so that a homogenous fusing can take place. Then 
hemolysis, through the influence of mechanical or chemical injury to the endothelium may 
take place, the hemoglobin of the red blood cells may disappear, and their stromata left as a 
colorless, dense reticulum. In such agglutinates, platelets and leukocytes then degenerate 
and form foci for the production of fibrin clots. Such stagnant blood columns in small 
vessels and capillaries then have as a characteristic the rapid degeneration of all the cells 
implicated, and are thus differentiated from the stagnant blood in the cadaver. 

The compression of the erythrocytes and the necrosing influence of slowly flowing but 
stagnant blood with the concomitant degeneration of other cells, particularly endothelial 
cells, seem to be the essential factors in the genesis of stasis thrombosis. In this sense 
mechanical and chemical moments combine to produce the end-results. 

Red or mixed hyaline thrombi correspond to stagnation of the total blood. But color¬ 
less hyaline thrombi can develop in capillaries and small vessels without admixture of 
erythrocytes when tissue is injured, either through cold or long continued ischemia. In 
such case the residual leukocytes, the fibrin masses, and the transuded substances then form 
a hyaline substratum which is not unlike a hyaline urinary cast in form and genesis. Simple 
ischemia, even when of considerable duration does not cause thrombosis. In the local 
asphyxia of the fingers occurring after exposure in susceptible individuals, the vitality of the 
blood and tissues remains intact, only the flow is retarded. After excessive cold, there may 
be simultaneous death of the surrounding tissues as well as of the blood in the vessels, so 
that no vital exchange is possible; then, too, thrombosis is absent. Thrombosis takes place 
only when the remaining living tissues can exert their effects. 

As compared with the stagnation thrombi in the smaller vessels, those in the larger ones 
are not essentially different, except that the separation of the colorless elements is not so 
complete as to produce obturation with these alone. In larger vessels one occasionally sees 
gross clotting of blood, not unlike cruor, following sudden interruption of the circulation 
(as in ligation of the plexus pampini formis). A sudden cessation of the blood flow results. 
However, even in the larger vessels such red thrombosis is usually under the influence of 
undulating currents, as manifested by the grouping of platelets and leukocytes, within the 
coagula. These form smaller and larger conglomerates that are evidences of the effects of 
the current’s waves. 

It is believed that there is always a necessity for a certain quantity of ferment for the 
development of red stagnation thrombi in the large vessels. Simple compression or even 
invasion of a vessel with an obturating tumor mass may not produce thrombosis. 

Further observations speak for the immediate importance and relationship of local 
increase in ferments in the formation of stagnation thrombi. A primary thrombus as 
soon as it becomes obturating, may bring about a secondary red thrombus. This is also 
noticeable in the specific type of thrombi in thrombi-angiiti sobliterans where secondary 
thrombi of red type are apt to cap the terminations of the specific clot. By reason of the 
action of the ferments, these secondary clots may extend for varying distances into the 
vessels and even into their branches. The extent of the secondary red thrombi exceeds 
the primary pulsion thrombus. Appearances of the secondary clot, too, speak for the 


MECHANICAL TYPES OF THROMBOSIS 


117 


diminution in the amount of ferment as the clot recedes from its point of origin. Where 
the secondary coagulum is attached to the primary thrombus, it is firmly connected, whilst 
farther away it tapers out and gradually shows an imperceptible transition into the fluid 
blood. 

In short, the origin of red stagnation thrombi is traceable to two principal factors— 
firstly, a weakening or deficiency in circulation and secondly, the presence of substances in 
loco that further fibrin clotting. 

Pulsion Thrombosis.—This is the most frequent form of human thrombosis, and was 
first given complete study by Zahn, 1 who called attention to the relationship between 
the wave motion transmitted in the pulse and the conformation of thrombi. 
\ irchow, von Recklinghausen and Zahn, therefore, were the founders of the mechanical 
theory. They conceived that retarded flow, whirlpool or eddy formation and undulatory 
movements were possible factors in thrombus formation. The participation of blood 
platelets as important components of white thrombi was first called attention to by Osier 2 



Fig. 41.—Schematic representation of stratified formation of thrombi reproducing the'wave 

currents. ( Beneke) 

and Hayem. 3 Pure platelet thrombi are not common in the human organism. They occur 
only there where the platelets can stick together and form firm masses, whilst the depo¬ 
sition of leukocytes and fibrin is prevented by the current. These conditions obtain 
where there is a strong current, particularly in arterial territories, as for instance, over 
areas of aortic sclerosis, aneurism, etc. In the venous channels leukocytes can become 
attached by reason of the diminished flow and agglutinate. Platelet thrombi are very 
often seen in the furrows in the arterial walls over atheromatous ulcers. There¬ 
upon the blood stream may model such thrombi. They cover the arterial wall with 
protecting hyaline covering and later may become calcified. 

White thrombi made up of platelets and leukocytes, with or without fibrin, are more 
common than the pure platelet thrombi. They begin with the deposition of the platelets; 
then occurs the attachment of leukocytes and fibrin. 

The most important forms are the wave and whirlpool or eddy thrombi. The aggluti¬ 
nated cells lie in the nodal points of the waves and in the centers of the eddies. According 
to the intensity of the blood stream they may be dense and narrow, or they may be loose 
and broad. 

The deposition of fibrin then follows by reason of the participation of the degenerate 
leukocytes. The agglutinates forming in the retarded stream lie in the nodal points of the 

1 Zahn, Virchow’s Arch., LXII, 1875; also XCVI, 1884, and CII, 1885. 

2 Osier, Ztschr., f. med. Wissensch., 1882. 

3 Hayem, Recherches sur l’anat. norm, et path, du sang, 1878. 




118 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


waves and in the centers of the whirls. Even the very smallest agglutinates show deposits 
of leukocytes. All the various degeneration forms can be seen, namely, detached granules 
of platelets, karyorrhexis, breaking down of the nuclear substance—are noted. Because of 
the large number of leukocytes one gains the impression that chemotactic influences attract 
them. The participation of leukocytes is of importance for the growth of the white 
thrombi in typical formations, in which a central agglutinate free from nuclei forms, 
and about which there is a zone of leukocytes. The breaking down of leukocytes goes hand 
in hand with the deposition of tissue material. 

Fibrin formation follows the chemical participation of degenerating leukocytes, beginning 
from the degenerating center. Fibrin threads surround the centers, and attain their great¬ 
est size between two coagulating centers. Histologic pictures are often observed which 
correspond accurately to the wave conditions present. Thus one finds at intervals more or 
less oblique masses of thrombus made up of platelets and leukocytes corresponding to the 
nodal points. Between these one finds the fibrin threads like water plants taking the direc¬ 
tion of the stream, and whose obliquity and curve depend upon the strength of the lateral 
pressure of the current. Lamella formation is another product of the mechanical hydro¬ 
static conditions. The parallel formations are due to repeatedly new depositions in the 
nodal points in a direction perpendicular to the current. This forms the reef-like surface 
of thrombi being a replica of the wave current (Fig. 41). 

The erythrocytes only play a subsidiary role in the process. When they are included 
between the layers of fibrin, they may persist for a long time without degenerating. They 
may be absent between the layers, as in the case of the white thrombi, which arise in the 
plasmatic part of the stream. Only then when the strength of the stream becomes so 
diminished that the peripheral portions of it are stagnant, and the erythrocytes also taken 
up in the wave thrombus, just as in the stagnation thrombus, then are produced those 
peculiar mixtures of red and white layers or mixed stratified thrombus (Fig. 41). 

In the mechanically produced thrombi the process sets in through agglutination of the 
platelets and the secondary fibrin formation and leukocytic accumulation that results from 
the autolytic poison. Therefore, to a certain extent even the mechanical thrombi are of 
chemical origin. The active substances causing the thrombosis emanate from the midst of 
the stream and from the constituent elements of the blood aided by the absence of inhibiting 
influences. The inhibiting influences under normal conditions are the constant dilution 
of the toxic substances in a normal blood current, and the checking action of the vessel wall, 
both of which are disturbed when mechanical influences are at work. 


CHAPTER XX 

THROMBOSIS OF CHEMICAL ORIGIN 

By true chemical thrombosis we designate those forms in which the plug 
formation arises by reason of chemical influences that penetrate from without 
through the vessel wall, or that are carried by the blood. Several varieties 
of thrombi are thus formed, the so-called spodogenic thrombi due to preci¬ 
pitation, and fibrin forming or agglutinating types. Fluid substances 
diffuse rapidly in the blood and have a general effect; more solid substances, 
by reason of their concentration, act locally and mechanically on the blood 
and vessel wall. 

Amongst chemical influences are included fluid and solid chemical agents, effects of 
general blood intoxication (from endogenic and exogenic poison), with injury of the vessel 
wall, and also thermic and actinic factors. 

Substances injected into the veins experimentally for the production of thrombosis, 
naturally exert their effect upon all the blood elements, although they may specifically 
alter certain elements more than others, particularly the erythrocytes. Injection of ox 
blood serum into the veins of rabbits produces fatal agglutination in the lung vessels. 
Hirudin injection does not prevent such agglutination which indicates that this process is 
not a fibrin coagulation. Fibrin formation has been produced experimentally in dogs by 
the injection of foreign serum. Hirudin injection prevents death by inhibiting fibrin 
clotting. 



THROMBOSIS OF CHEMICAL ORIGIN 


119 


Other forms of blood clotting have been experimentally produced through the injection 
of substances, that either destroy the blood corpuscles at once, or break them up (spodo- 
genic thrombi), or that cause precipitation thrombi by granular deposition of the soluble 
albuminoid substances in the plasma (Dietrich 1 ). Von Bardeleben 2 found that even rich 
cultures of streptococci when introduced into the blood, did not cause thrombosis, but 
only when stasis was caused in a vein in which cocoi were developed. 

Dietrich, when he injected hemolytic agglutinating or precipitating substances into the 
blood stream, encountered typical seggregations or platelet thrombi whenever the blood 
stream was diminished in intensity. 

The simultaneous injection of chemicals and injury to the vessel wall is especially effec¬ 
tive through the latter agency. With complete necrosis of the vessel wall the hyaline and 
static type of thrombi develop (stagnation thrombi). More mild degrees of vessel injury 
cause thrombus formation corresponding to the pulsion type, insofar as they are derived 
from agglutinates of platelets and develop into white thrombi. The removal of the vital 
function of the endothelial cells alone leads to agglutination thrombosis, whilst simul¬ 
taneously cooperation of fused toxic substances may lead to precipitation or to 
agglutination. 

In the larger arteries the same insult ( e.g . caustics) are not so apt to cause thrombosis as 
in the veins, in which agglutinates are more likely to adhere. The degree and the nature of 
the mural changes are important for the origin of thrombi. Whenever reaction is present 
in the walls, particularly with fibrin formation, the conditions for thrombus deposition are 
present. On the other hand, when the toxin diffuses, precipitates or agglutinates are more 
apt to form. 

Inflammatory Processes.—Hyaline thrombi often accompany inflammatory processes, 
So long, however, as the inflammatory irritation of the vessel wall does not interfere with its 
vital functional capacity, thrombosis may be absent. Even accumulating leukocytes may 
not give rise to thrombosis, and it is not until these necrose and degenerate that thrombosis 
ensues. When, by virtue of specific action, fibrin deposition occurs in the lumen, then 
thrombosis immediately occurs. 

In the larger vessel fibrin formation may occur within the vessel wall and layers. This 
may extend into the vessel lumen. Then thrombosis occurs. It is easily understood that 
inflammatory exudation of fibrin on the inner surface of the vessel wall would be relatively 
stronger when the current is slow, as in the veins. This is in accord with the more frequent 
combination of thrombosis with phlebitis than with arteritis. Talke 3 was able to produce 
obturating thrombosis in the sheaths of vessels in which staphylococci were inoculated. 
The thrombi were probably evoked through the diffusing toxins, and the bacteria secon¬ 
darily entered these clots. At first platelet deposits were noted by this author, and later, 
red or mixed clots. 

In the case of staphylococci it has been found more difficult to produce such thrombosis, 
other factors being necessary such as marked retardation of the stream. Other authors 
were able to produce thrombi, with the injection of bacterium coli in the walls of the vessels. 

In all of these experiments it is not the specific toxins of bacteria that predispose to 
thrombus deposition, but the total inflammatory exudate with its plasmatic, fibrinous and 
leukocytic accumulation, that evokes fibrin coagulation and platelet agglutination. 

Chemical Varieties. Endogenous Poisons .—In extensive burns poisons 
are doubtlessly formed in large quantities, in contiguous tissues. Their 
absorption can be regarded as the cause of death. It has not been decided 
as to what role these poisons play in the production of thromboses in the 
organs. Thrombi, indeed are found in the form of hyaline masses in the 
small vessels and capillaries of the organs, particularly in the stomach and 
duodenum, sometimes associated with small peptic erosions. Aschoff 
reports small white thrombi in the lung arteries in a case. A thrombophilic 
tendency after burns, as an expression of the general intoxication, has not been 
proven. 

In eclampsia there is a characteristic predisposition in certain organs to 
th e formation of autochthenous capillary thrombi. Perhaps certain chemical 
local changes including degeneration of red and white blood cells in the liver, 
or the protagon and cholesterin contents in the brain, lungs and kidneys, are 

1 Dietrich, Path. Zentralbl., 1912, XXIII, 10. 

2 Von Bardeleben, Arch. f. Gynec., 1907, LXXXIII. 

3 Talke, Beitr. z. klin. Chir., 1902, XXVI. 


120 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

the factors that increase tendency to thrombosis. The increasing leukocy¬ 
tosis of pregnant women has been regarded as a morphological expression of 
a particular status of intoxication, perhaps of ferment production. On the 
other hand, it is well known that the coagulation time is not notably changed 
in pregnant women, nor is the cadaveric blood of eclamptics more prone to 
clot. It is believed, therefore, that whatever thrombosis occurs in such cases 
is rather due to an intensive local chemical action in which lipoid substances 
play a special role. 

The occasional occurrence of sinus thromboses or similar implication of the. lung arteries 
in children suffering from severe dysentery, has been explained on the supposition that there 
is absorption of poisons from the intestines. Circulatory weakness, however, is more 
important in these cases. Here, just as well as in the thrombi associated with carcinoma 
cachexia, it is found that the thrombi correspond in structure to the mechanical pulsion 
thrombi, and not to the experimental intoxication thrombi. ... 

The so-called ferment intoxication can be brought into play through injection of 
defibrinated blood of the same species, through foreign blood, or special ferment solutions. 
It has been known for a long time that foreign blood as well as tissue extracts produced 
clots, a condition most apt to occur in the large blood vessels. 

When tissue extracts are introduced into the circulation, sudden death from intravascu¬ 
lar coagulation may result. An albuminoid substance, foreign to the blood, and not the 
precursor of thrombin, is believed to be found especially in the tissues. 

Fibrin ferment in solution such as serum has been shown by Dienst to cause sudden 
death in rabbits through embolism of the lung with coagulation in the right heart. Small 
quantities produced very toxic injuries to the parenchyma of the kidney, up to necrosis 
with the formation of hyaline and platelet thrombi in the capillaries. 

Exogenous poisons, such as ether, benzol, chloraform, pyrodin, ammonia, 
potassium chlorate, amyl nitrite, ricin, etc. have been known to bring about 
similar results. As for the influence of bacterial poisons—Loeb reports 
formation of red thrombi following injection of staphylococcus toxins. 

The Action of Exogenous Poisons and Infectious Agents .—Changes in the 
total blood in the sense of increased coagulability are rare. Extensive cruor 
formation in most of the vessels is seen post-mortem after carbon monoxid 
poisoning. After transfusion of foreign blood lethal clotting has been 
observed. In eclampsia, anemic infarcts have been observed in the kidneys, 
due to hyaline thromboses with a picture of anuria. In the transfusion of 
foreign blood hemolytic processes leading to ferment over production and 
to local accumulation of erythrocytic fragments may occur. Thrombi of 
various types appear in the capillaries in various types of poisoning (bichlor¬ 
ide and anilin). 

All poisons that act in a destructive way upon the blood, do not necessarily 
lead to thrombosis. Thrombosis is absent in the cases of methhaemoglo- 
binemia after potassium chloride and nitrite poisoning. 

As a rule the larger parasites do not cause thrombosis when they are 
found in the blood. The trypanosomes, even in large numbers, do not lead 
to clotting. This is also the case with bacteria. Even when there are 
atheromatous ulcers, bacteria do not seem to further the deposition of clots. 

The presence of bacteria does not essentially modify already existing 
mechanical thrombi, such as occur at points of ligation in the placenta. 
One would expect a favoring influence upon the growth of bacteria by reason 
of the presence of a clot, but indeed it is noted that bacteria are sometimes 
inhibited in their proliferation by just such a thrombotic process. 

One may conclude, therefore, that infection with a variety of different 
bacteria does not suffice, as a rule, for the creation of thrombosis. Even in 
diseases such as fibrinous pneumonia in which conditions are present that lead 
to a saturation of the blood with fibrin ferment, thrombi are not so frequently 


THROMBOSIS OF CHEMICAL ORIGIN 


121 


found as one would expect. When, however, bacteria such as streptococci 
invade the lumen of vessels in considerable number, fluid pus develops in 
veins very frequently without thrombosis. Sometimes such pus is separated 
from the current through a clot. Thus, we may conclude that the bacterial 
contents of the blood and bacterial poisons are not essential for the origin of 
thrombi in infection. Septic thrombosis is produced rather by disease of the 
vessel wall. 

In atheroma Lubarsch does not consider the intima changes as playing an 
important part in thrombus formation. When the current is strong, thrombi 
rarely become attached to such patches. When there is mere fatty degen¬ 
eration of the endothelium, thrombosis is usually absent. Even extensive 
change in the vessel wall, such as amyloid alterations of a large vessel or 
capillaries, does not necessarily lead to thrombosis. Chemical factors are 
however, important when smaller or larger vessels suffer necrosis through the 
action of poisons. Essential for thrombosis, therefore, would be the presence 
of diffusible poisons that enter the blood and modify it; or an active partici¬ 
pation of an altered vessel wall through unusual special responses. In 
some cases the injury to the blood elements through the vessel wall is a chief 
factor; as following the injection of poisonous substances, or following the 
action of strong poisons through surface defects. 

The form of thrombosis then varies according to the peculiar character¬ 
istics or qualities of the toxic substances. Thus, in the case of acid poisons 
entering through the stomach, such as sulphuric acid, a sort of stasis thrombo¬ 
sis occurs, with distension of the capillaries and smaller vessels with red 
thrombi. Or, in the case of putrid cystitis or pyelitis, hyaline thrombi occur 
in the neighborhood of ulcers and degenerate tissues. 

In clinical pathology most interesting are the local vessel wall infections, 
particularly of the veins. A vein that is inflamed with staphylococci and 
streptococci shows the same leukocytic infiltration as any other tissue. With 
this a fibrinous excretion within the walls takes place. The process may be 
limited to the wall itself, particularly when only the adventitia is involved, 
the blood flowing within the vessel without being affected. When the fibrin¬ 
ous deposition is more diffuse, and enters the inner layers of the wall of the 
vessel, then platelet masses become attached to the intima. It is believed 
that the fibrin masses combine with the platelets, and can be traced to com¬ 
municate directly with the intramural fibrin deposit. Most of the fibrin, 
however, has its origin in the flowing blood and does not emanate from the 
vessel wall. As the thrombus grows, it presents a mechanical obstacle to 
flowing blood, and there results the usual wave and eddy formation with cor¬ 
responding mechanical accumulation of new thrombus masses. 

Infectious processes vary in their influences on thrombus formation. 
Whilst thrombosis is seen in the superficial veins in syphilis during the preco¬ 
cious form of syphilitic migrating phlebitis, it may be absent in the umbilical 
veins, even though circulatory conditions are favorable for clotting. In the 
secondary stage, with endo- and periphlebitis syphilis does produce thrombo¬ 
sis (Hoffmann, Chap. LXXX). In tuberculosis extensive phlebitis migrans 
has been seen to occur without thrombus formation (Schwarz 1 ). Glassy 
masses are known to fill the veins in the neighborhood of severe diphtheritic 
lesions, an expression of the reaction of the circulating toxins. 

The tubercle bacillus may develop nodules in the vascular wall (vessel wall), which may 
later give rise to mechanical thrombus deposition (Benda 2 ). But, even here the thrombus 

1 Schwarz, Virchow’s Arch., 1905, CLXXXII. 

2 Benda, Berl. klin. Wchnschr., 1908, XLV, 7. 


122 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

formation is usually rather insignificantly organized. Parietal thrombi were seen in the 
case of Beneke where there were about a dozen such deposits in a number of veins oi the 
lungs. They had the appearance of droplets that had become congealed as they flowed 
along the wall in a central direction. 

In meningeal tuberculosis, however, the thrombi caused by fresh tuber¬ 
cles in the pia usually are obturating. . 

In the inflammatory diseases of the arteries, with the exception of thrombo¬ 
angiitis obliterans, thrombosis is not as common as would be expected. 
Inflammation of the vessel wall, as a rule, only produces thrombosis then m the 
large vessels, when mechanical deposition is facilitated through changes m 
contour, such as aneurismatic dilatation. A very striking type of thrombus 
formation is that of periarteritis nodosa (Chap. LXXIX) or polyarteritis. 
Here foci of intensive inflammation develop in the smaller vessels, leading to 
destruction of the vascular wall. As soon as the intima is reached, aneuris¬ 
matic dilatations occur With thrombosis. Fibrin, leukocytes and hyaline 
masses occupy the clot. Destruction of the arterial walls furthers the throm¬ 
bus formation. In the veins the circulatory sluggishness; in the arteries 
transitory vasoconstriction with consequent fibrinous deposits, are factors 
that predispose to thrombosis. ^ 

In the case of capillaries in an inflammatory area, leukocytes may clog 
their lumina and lead to the formation of hyaline, masses. This occurs in 
pneumonia, in which glassy thrombi are characteristic. 

Thrombosis Due to Solid Bodies.—Here we deal with the blockage of vessel lumina 
through migrated body constituents, with or without bacteria, as well as intravascular 

P In fat embolus there is but little tendency to thrombosis. In the neighborhood of 
fractures, the veins may contain fluid fat that is held fast by thrombi. Air (air embolus) 
does not incite clot formation. . ... ... 

Normal tissues have not identical chemical actions. We deal usually only with solitary 
cells (placentar). These circulate and do not act in a deleterious fashion on the blood 
elements. When they die off, the injury produced is so minimal as to exert no thrombotic 
effect. Where larger fragments of tissue, such as pieces of liver, are mechanically displaced 
after liver traumata, the action is mechanical. 

The displacement and the distant transportation of material containing ferment, such as 
detached thrombus particles, produce much more extensive additional thrombosis. Trans¬ 
ported thrombi by reason of their ferment properties, predispose to further coagulation, and 
after death are even known to be the points of origin of fresh cruor masses. Very long 
secondary thrombi are often attached to such emboli, an evidence of their chemical action. 

Thrombosis Due to Thermic Influences.—Thermic forces are exerted 
through injurious action on the blood itself, or through lesions of the vessel 
walls. Both heat and cold can produce thrombosis. 

The general effect of extensive burns has been regarded as an expression 
of blood destruction due to ferment intoxication and attended with extensive 
blood coagulation. Other authors deny that extensive coagulation takes 
place. It is believed that large quantities of ferment are developed at the 
site of the burn, enter the blood and cause thrombosis. 

The observations in the human conform to the experimental investiga¬ 
tions. In the case of extensive burns the picture of intoxication preponder¬ 
ates over the thrombotic lesions. 

Mild degrees of heat lead to hyaline thrombi in the affected locality. The clots fill the 
vessels, inflammatory reaction of the vessel wall being absent. Probably congelation of the 
dead leukocytes produces the plugs here. In the capillaries and small veins, at the margin 
between dead and healthy tissues, thrombi are not infrequently found. In some cases the 
clots have been regarded as precipitation phenomena. 


GENERAL CAUSES OF THROMBOSIS 


123 


Effects of Local Refrigeration .—The experiments of Zahn 1 showed that 
cold produces stasis and then thrombosis in the arteries, veins and capillaries. 
Experimental freezing in rabbits and guinea pigs demonstrated the develop¬ 
ment of typical inflammatory pictures. True thrombi do not necessarily 
form, but when the leukocytes attracted in this process, are caused to die off. 
Then these are converted into hyaline masses; and, together with the fibrin 
they fuse into masses that are regarded as thrombi. Even the vessel wall, 
when the action of cold is intensive, may participate in the degenerative proc¬ 
ess, become hyaline, and fuse, as it were, with the thrombus. In this way, 
extensive congelation thrombi may form in the region of the frozen area. 
In the necrotic areas themselves, the thrombi may be absent, being confined 

to the marginal zone between healthy and dead tissues. 

0 

The longer the cold effects are allowed to act upon the tissues, without direct necrosis, 
the more the circulation is impaired, and the more extensive the formation of hyaline 
thrombi. The circulatory conditions are determining factors in many cases. It has been 
shown that experimental section of the sympathetic nerve in the necks of rabbits was 
followed by more marked thrombosis than in those in which the vascular nerve mechanism 
was intact. 

Thrombosis Due to Actinic Causes. —Electricity, X-ray and other actinic 
influences seem to exert about the same effect upon the blood and tissues as 
thermic insults. Local thrombi are caused by these whenever their action is 
sufficiently intensive to produce necrosis in blood or tissues. Jansen 2 describes 
local thromboses after light treatment; and Askanazy 3 observed thrombosis 
after the use of ultra-violet rays. 


CHAPTER XXI 

GENERAL CAUSES OF THROMBOSIS 

Thrombosis may depend (i) on factors inherent in general diseases; (2) 
on local mechanical or chemical alterations; and (3), on special conditions. 

1. Thrombosis and General Diseases. —Beneke in his excellent work in 
this field proposed a grouping into general mechanical and chemical 
causes. 

Cardiac weakness, whatever may be its origin, is an important factor. 
This may be brought about by toxic and infectious degeneration, excessive 
stress through stenosis, valvular insufficiency, or local disease of the cardiac 
muscle, as well as through senile change. In many of the post-operative 
thromboses and the marantic group, such conditions play a role. For, the 
clotting is most apt to take place where circulation is sluggish, as in the venous 
system, or where waves and vortices are likely to occur. 

Local stasis, too, may be regarded as a contributing cause and with general circulatory 
weakness eventuates in thrombus formation. Indeed, Beneke states that ligation or tumor 
invasion of large veins need not give rise to this process until marked stasis occurs as the 
result of cardiac weakness. 

Changes in the character and form of the stream, associated with currents interrupted by 
vortices and waves are important forces making for thrombosis. Examples are varices, 
aneurysms with variations in the size of the arterial lumen, sclerosis of the coronary, 

1 Zahn, Loc. cit. 

- Jansen, Ziegler’s Beitr., 1907, XLI. 

3 Askanazy, Pathol. Anat., (L. Aschoff), Fischer, Bd. 1, 1919. 


124 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


cerebral, and popliteal arteries. If a sudden alteration in the lumen is met by the flowing 
blood, eddies and vortices ensue, which with other agents such as cardiac weakness or 
special local muscular demands, may lead to thrombosis. 

All these aforementioned factors are potent in proportion to the weakness 
of the general circulation. And so the preponderance of venous thrombi 
over the arterial is explained. Conversely, a strong current will inhibit 
thrombus formation. 

Although the mechanical forces may suffice to generate thrombi, the latter may fail to 
develop where all the conditions for their production seem at hand. Hence qualitative and 
quantitative alterations in the blood corpuscle elements and their chemical relationship to 
the plasma, have been invoked in explanation. These possible motivating agents may be 
summarized as (i) anomalies of the blood cells including increase or diminution in the 
number of erythrocytes or platelets, leukocytosis and leukopenia 5(2) anomalies of the plasma 
such as altered carbon dioxid, calcium ions, fibrinogen, fibrin ferment content; and (3) 
diverse conditions, such as increased agglutinability of the platelets, effects of age, 
cachexias and infection. All these may be of chemical nature. 

Although it is often impossible to gauge the importance of chemical fac¬ 
tors in a given case, the following brief summary may help clarify our inter¬ 
pretation of etiology. 


The Alterations in Corpuscular Elements. —An increase in the number of erythrocytes 
seems to have no essential influence on thrombus formation. Polyglobuly or plethora may 
cause disassociation or separation of plates and thereby diminish the tendency to clot. 
A superadded factor, however, such as cardiac weakness, may nullify this and thrombosis 
nevertheless supervene. 

A diminution in the number of red blood cells (erythropenia) may further the clotting 
process by an association of factors. Perhaps the diminution in the size of the vascular 
marginal zone in erythropenia may be a mechanically conducive element. To the coinci¬ 
dent numerical increase of platelets must be also ascribed a certain role. So also, has been 
explained the mechanical thrombosis occuring in anemic persons. However, there is not a 
great tendency to thrombosis in anemic conditions, unless cardiac weakness is added as a 
factor. 

In chlorosis, however, we have an exception, in that the inferior vena cava, the crural 
and renal veins are reported as being more than ordinarily predisposed to thrombosis. 

Leukocytosis is a condition which theoretically would favor thrombus formation. 
Beneke believes that this could occur through deposition of leukocytes at any platelet 
center, and through the elaboration of ferments. 1 And so in leukemia the frequency of 
thrombosis has been especially noted (thrombosis of corpora cavernosa in priapism). 
Whether there is an overproduction of fibrin ferment, as has also been suggested by Dienst 2 
in eclampsia, has not as yet been definitely proven. Leukopenia does not seem to influence 
thrombus formation. 

Increase in the number of platelets has very frequently been recognized as conducive to a 
state of thrombophilia. Some of the post-operative thrombi occurring 4 to 5 days after a 
severe loss of blood, at a time when platelet production is most intensive, has been regarded 
as due to this phenomenon. It has not been satisfactorily proven, however, that a platelet 
increase per se is a cause of thrombosis. Diminution in the platelets, similarly, in severe 
anemias and acute febrile conditions does not explain tendency to thrombosis. 

2. Chemicab Alterations of the Total Blood.—The carbon dioxid content of the blood 
may inhibit coagulation by reason of the altered sensibility of the platelets, for these are 
said to degenerate through such chemical changes in the blood. In spite of this chemical 
restraining element, conditions in which there is increased carbon dioxide in the blood, such 
as stasis, show an increased tendency to thrombosis, due to the fact that the mechanical 
conducive moments more than counterbalance the chemical inhibitory. 

The Ca- Ion content of the blood has been regarded by some authors as important in 
thrombus formation. 

1 See the case of Dr. G. in whom extensive obliteration of the vessels of the lower 
extremities, probably due to thrombosis had occurred, and in whom leukocytosis was 
present for many months and possibly years without known cause (Chap. LXXXII). 

2 Dienst, Archiv. f. Gyn., 1912, XCVI, 1. 


GENERAL CAUSES OF THROMBOSIS 


125 


The fibrinogen content, according to Welch and Aschoff is not responsible for altered 
susceptibility to thrombosis. Of more importance is the fibrin ferment content of the 
blood. Sudden increase of this element in experiments causes extensive clotting in the 
large vessels and immediate death. This lends confirmation to the view that excessive 
local ferment production may enhance thrombus formation. In the circulating blood 
neutralization or the destruction of ferments goes on constantly. The experiments of 
Dienst would indicate that in some cases sudden, in others a more or less continuous, 
overproduction of ferments may occur. 

Cases are reported of extensive sudden thrombosis following small, mini¬ 
mal, primary, mechanical thrombi, and requiring but a very few minutes for 
their development. Two cases are cited in menstruating women. In one of 
these after a clean appendectomy, sudden coagulation of the blood in the 
inferior vena cava took place, resulting in pulmonary embolism and death 
within a few minutes, in the other case a red thrombus in the uterine veins 
seemed to be the starting point. In both of these, the authors concluded 
that there was sudden invasion of the blood with fibrin ferment, that enabled 
a very small mechanically produced thrombus to give rise to extensive coagu¬ 
lation. Mixed thrombus formation over a large territory has been reported 
in chronic nephritis where a more or less continuous state of increased ferment 
production was assumed to exist. 

In the extremities we have not infrequently observed the association of 
extensive red thrombosis with emboli after infectious diseases and pneumonia. 
The suddeii extension of thrombus formation throughout all the larger arteries 
and veins does not always occur in various embolic processes. Indeed, the 
absence of such secondary thromboses in most of the cases of arteriosclero¬ 
tic blockage is noteworthy. The frequency thereof is striking in the above 
mentioned cases. Perhaps here, too, an overproduction of fibrin ferment, is a 
factor. 

3. Special Conditions. —Little is known regarding the influence of 
increased viscosity as a factor in thrombosis. Increased viscosity of the 
blood is said to take place with increasing age, 1 and in certain infectious 
diseases (tuberculosis and pneumonia). 

Welsh found no direct relation between coagulation time and viscosity. 2 
Holmgren, 3 however, takes the view that the polymorphs influence viscosity 
and the latter coagulation. His experiments tend rather to show a relation¬ 
ship between the polymorph content or polymorphlymphocy te quotient, than 
upon viscosity of the blood per se. 

Except in the case of cholera, in which concentration of the blood follows 
the withdrawal of water, no particular tendency to mechanical thrombosis 
has been observed in conditions with increased viscosity. 

The relation of thrombosis to age, has given rise to much specula¬ 
tion. The chemical differences in the blood and the quantitative relation of 
the platelets and the changes in the vessel wall have all been regarded as 
factors in the tendency of adults to thrombosis. That cardiac weakness may 
be a factor in the senile cases must be admitted. Nevertheless chemical 
alterations must not be lost sight of, and are probably of considerable impor¬ 
tance. 

In the thrombosis of cachectic conditions and in the marantic conditions, 
the quantity of blood and its composition, or the chemical relationship 
between the corporal and fluid elements have undergone change. Pathological 

1 Hess, Deutsch. Arch f. klin. Med., 1908, XCIV, 404. 

2 Welsh, Heart, Vol. Ill, 1, 1911. 

3 Holmgren, Deutsch. med. Wchnschr., Jan. 30, 1913. 


126 CIRCULATORY AFFECTIONS OF TIIE EXTREMITIES 

products of metabolism circulate in the blood, or the blood is depleted of 
certain substances. Malignant cells may have a special affinity and attrac¬ 
tion for blood components. 

In the present state of our knowledge we must admit the possibility of a chemical 
component in the production of the marantic thrombi. Only in this form is their depen¬ 
dency upon mechanical forces brought to our notice. 

The Rdle of Infection in Thrombosis .—Infection can indeed play an impor¬ 
tant part in thrombosis. According to some authors this is due to an exten¬ 
sive vasculitis. Inflammatory foci with or without bacilli in the vessel wall, 
and the action of toxins have been regarded as the causes of parietal or other 
thrombi in typhoid fever. Systematic investigation of the occurrence of 
endophlebitic foci in the various infectious diseases has given rather negative 
results. The evidence seems to show that although focal infection of the 
walls of the vessel cannot be denied in infectious processes, no important 
role can be ascribed to these lesions in usual thrombus formation. The occlu¬ 
sive thrombosis in certain special types of phlebitis of unknown origin and in 
thrombo-angiitis is an exception (Chap. LXXXI). It would appear that 
the direct effect of bacteria and their toxins upon the total blood (or the 
forces engaged in circulation) are more important. The cardiac degeneration 
brought about by infection affords one of the mechanical conditions. So also, 
the existence of other coincident conducive agents cannot be denied. 

Aschoff points out that embolic infarcts even in sepsis are not necessarily bacterial, but 
frequently agglutination thrombi with secondary invasion of organisms. Up to the present 
time we are unable to properly estimate the effects of the various chemical components of 
infection upon the alterations of the fibrinogen, the fibrin ferment; on the increase in 
number of leukocytes and platelets, the erythrocytes and their degeneration. Nor do we 
know whether specific agglutinins (platelets) are produced. Indeed, experimental methods 
have shown that certain toxins and bacteria have a specific action upon certain parts of the 
total blood. If we accept the theory that the essential moment in thrombosis is the coagu¬ 
lation, the absence of thrombi in many cases of hemolytic streptococcus infection and the 
frequent development of thrombi in pneumonia or staphylococcus infection could be 
explained on a specific toxin effect. Such assumption, however, cannot be admitted as yet, 
since thrombosis is not merely a process of coagulation. ... 

Even the possibility of a diffuse chemical influence of infectious poisons upon the vessel 
walls has been considered, and paralysis of the inhibitory activities of the endothelial cells 
in so far as these have a defensive mechanism against thrombosis. These, however, are 
speculative theories. 

Although infection can thus play a role, it is not necessarily followed by 
thrombosis, unless some other special factor is brought into operation. 

Mendel 1 suggested the appellation “ thrombophilia” to designate a general 
predisposition on the part of a patient with infectious disease to thrombosis. 
This was extended to include that state of heightened susceptibility to throm¬ 
bosis that may occur after an infection has been overcome. Such an acquired 
state would be opposed to hemophilia in which an absence of thrombokinase 
has been believed to occur. There is still some doubt as to the correctness 
of this assumption. 


Various causes 2 have been given for the tendency to thrombosis in infection. Very few 
cases of thrombosis occur in the cadaver in which we are not able to demonstrate an infec¬ 
tious malady of some sort as a possible cause, (i) Thrombi are particularly frequent in 
the neighborhood of infectious processes; (2) in varices, the blood is apt to remain fluid as 
long as infection in the neighborhood is absent; and whenever a wound in the skin permits 

1 Mendel, Miinchen. med. Wchnschr., 1909, LVI, 42. 

2 Lubarsch, Berl. klin. Wchnschr., March 11, 1918. 


GA NGRENE—GENERA L CON SID ERA TIONS 


127 


of the entrance of bacteria, thrombosis occurs; (3) in post-operative thrombosis, there is 
usually associated elevation of temperature; (4) microscopic search and bacteriological 
cultures of thrombi have demonstrated the presence of bacteria; and (5) it has been found 
possible to produce thrombi in animals by the injection of bacteria. 

Kretz states that of 6511 cases he was unable to find a single instance in which thrombus 
formation was not associated with previous infection. Lubarsch, on the other hand, in his 
material notes 13 per cent of thrombi in which no infectious process could be discovered. 
If the remaining number (87 per cent) is critically reviewed for a possible regional relation¬ 
ship between the infectious process and the thrombosis, it appears that only 55 per cent 
showed any association, and these would have to be still further reduced to 52 per cent if 
thrombi are excluded that might have antedated the infectious process. 

Autopsy material then would suggest that the infectious process plays a considerable 
role in about half of the cases. 

How can the action of bacteria be brought into harmony with the usually accepted 
theories as to the genesis of thrombosis? Firstly, the influence of the infectious agent upon 
the heart and the circulatory centers; secondly, on the blood and the blood forming organs, 
particularly the bone marrow; and thirdly, the action on the blood vessel wall:—these are 
the theories that have been advanced. 

If we emphasize the role of alterations in the blood constituents as a determinant in 
thrombosis, the action of organisms in a chemical and morphological sense can be easily 
brought into consonance with existing theories of thrombus formation. Thus, bacteria 
not only destroy the red blood cells, but also through their action on the bone marrow, 
particularly on the giant cells (megakaryocytes) may play an important part. Both red 
blood cells and giant cells are influential in the formation of blood platelets, be they con¬ 
sidered as products or degeneration products. For, it is known that giant cells are thrown 
out into the blood stream by reason of irritation by bacteria, so that the influence of strepto¬ 
cocci, for example, can easily be understood both on the basis of their destroying influence 
on the red blood cells, as well as on the basis of their irritative effects on the bone marrow. 


CHAPTER XXII 

GANGRENE—GENERAL CONSIDERATIONS 

Gangrene (Fr., gangrene, Latin gangraena, from Greek 7 ayypcava an 
eating sore ypaw, ypaeiv to gnaw) signifies the death of macroscopically 
visible portions of the body, the invisible liquefaction of tissue being known 
as molecular death or ulceration. 

Mortification is synonymous with gangrene, being more frequently used in 
the parlance of the laity. 

Mummification refers to that type of gangrene in which drying or desic¬ 
cation of the tissues takes place. 

Sphacelation means total death of all of an affected part, the dead tissue 
being known as a sphacelus. 

Sloughs are dead masses of tissues, the result of a process of sloughing. 
The act of sloughing which results in the formation of sloughs may be brought 
on by ulceration or inflammation. Thus, a core is an inflammatory slough; 
when it is sufficiently large and possibly putrid, it is termed gangrenous 
slough. 

Properly speaking, necrosis is a general term that should include all types 
of tissue death. Although used in this way by the Germans, in English 
medical parlance, it is more frequently applied either to the disintegration or 
death of internal organs, when the mortification is unattended by decom¬ 
position, or to the death of bone tissue. 

Gangrene is usually the result of imparied or absent blood supply. Other 
causes, however, must be able to bring about mortification in the presence of a 



128 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

natent and apparently intact or adequate circulatory system, as in the so- 
caUecf vasomotor varies of gangrene of which Raynaud,. diseaseis an 
examDle. It is by virtue of the development of an adequate collateral 
circulation that gangrene can be prevented, so that we can distinguish 
between the clinical picture of impaired or arrested circulation with gangrene 
as a sequence, and where gangrene has been averted through the developmen 

of sufficient secondary circulatory paths. f 

In addition to the factors, impairment of circulation and establishment 
collaterals, other influences may determine the development.of gangrene^ 
These are the general condition of the patient and the local condition An 
enfeebled general condition, a weak heart, the debilitating effects o p o 
longed illness, of infection or diabetes, all these, not only lower the Jitahty, 
but also militate against recovery. Local conditions such as extra.vasa.tios 
of blood, inflammatory exudates, localized vascular disease, stasis or co - 
gestion resulting from tight bandages, and improper posture, are addition 
fmpediments to the formation of collateral paths. The tissues too, vary as 
to their vulnerability, the vitality of bone, cartilage, tendons and fascia being 
apparently greater than that of muscles and nerves, whilst the glandular 
organs and the elements of the simple nervous system seein to succumb 
within a very few hours after complete blockage of the main avenue of 
blood supply. In certain tissues, such as muscles and nerves, impairment ol 
circulation produces temporary ischemia, which, if not of too long duration, 
leads to degeneration, functional disturbances, so-called ischemic contracture 
and palsy, but not to gangrene. . p , _ 

For a thorough comprehension of the clinical manifestations of gangre 
or impending gangrene, it is essential to be able to recognize ? ot 
signs that appear when the condition is definitely and well developed, but all 
those objective evidences of impaired circulation that may precede by months 
or even years the advent of true gangrene or even of trophic disorder. Ihe 
signs and symptoms of gangrene and those of impaired circulation will be 
merely mentioned here, a detailed description being given under the dis¬ 
cussion of the various types of gangrene. , . 

Sims of death of a limited part are the following: first, loss of pulsation in 
the usually palpable vessels; second, coldness of the part; third, absence of 
sensation or paresthesiae followed later by anesthesia; fourth, loss of active 
motion in the part, or loss of function; fifth, change in outward appearance, 
chiefly in color. At first there may be intense blanching, the skin having a 
waxy, cadaveric or ivory tint. Or, if the part be engorged with blood by 
virtue of intense venous stasis, a cyanotic livid hue will predominate. Later, 
the color and appearance of the part will change, as the condition of dry or 
moist or mixed gangrene is developed. 

Premonitory Symptoms of Gangrene— These are best illustrated when the 
extremities are the seat of impaired or arrested circulation. It is quite as 
important to be cognizant of the objective and subjective phenomena antedating 
the advent of gangrene or trophic disorder, as it is ■ to recognize the death of tissue 
itself for, in most cases in the clinic, the diagnosis of the arterial lesion leading 
to gangrene should precede hy a longer or shorter period the onset of the gangrene 

Symptoms of Impaired Circulation. —Certain definite clinical manifestations 
of diminished blood supply are frequently the precursors of gangrene Or 
gangrene may occur in one limb and never develop in the other, although both 
fimbs offer the signs of diminished blood supply. The most important of 
such clinical signs are the following:— 


GA NGRENE—GENERAL CONSIDER A TIONS 129 

/ 

1. Intermittent Claudication .—By this term is meant cramp-like pains in 
the calf of the leg brought on by walking or running, and causing the patient 
to rest the limbs. The pain regularly disappears when the muscles are in a 
state of repose/" Less typical pain referred to the ball of the foot or the ankle, 
or the instep, must be regarded as of the same nature. Erb’s syndrome 
called “intermittent claudication” should not be regarded as a clinical 
entity, for the symptoms described as intermittent limping do not belong 
to any one group of cases, but occur in almost all of the cases in which 
obstructive or obliterative disease of the arteries of the lower extremities is 
present.Thus, intermittent claudication is a symptom of thrombo-angiitis 
obliterans/athero- or arteriosclerotic disease, arteriosclerosis with diabetes 
or with thrombosis, or endarteritis, and aneurysm of the popliteal artery. 
The feeling of weakness in the affected part also influenced by motion, prop¬ 
erly belongs here, since it is so frequently associated with the pain and 
cramp-like phenomena. Clinically similar manifestations may have been 
described (Dejerine) with apparently patent peripheral arteries where a 
lesion in the spinal cord is held responsible. 

2. Coldness of the extremity , when chronic, is a significant sign. It may 
be influenced by climatic conditions and intensified by exertion. It is 
manifested subjectively and objectively. 

3. Bluish discoloration {cyanosis) of the tips of one or more toes, particu¬ 
larly the great toe, sometimes of the ball of the foot, intensified by walking 
and associated with coldness—is another important manifestation. 

4. Ischemia or blanched condition of the extremity may occur when the 
limb is in the horizontal position, more rarely in the dependent, but can 
usually be elicited by elevating the affected limb 60 to 90° above the 
horizontal. 

5. Redness or rubor involving the toes, sometimes the dorsal and plantar 
aspects of the foot for varying distances (to the ankle or even higher), is a 
feature of diagnostic importance. It frequently involves the lower extremi¬ 
ties when these are allowed to hang down, occasionally occurring even in the 
horizontal position of the limb, and independent of infection, gangrene, or 
trophic disorder. The author has termed this phenomenon “erythromelia.” 

6. Absence of pulsation usually occurs in the palpable vessels of the 
extremities, the dorsalis pedis, the posterior tibial, popliteal, or femoral of the 
lower extremity, the radial, ulnar or brachial arteries of the upper extremity. 

7. Trophic disorders include indolent fissures, ulcers, hemorrhagic areas, 
superficial ulcers, perforating ulcers, a withered or atrophic condition of por¬ 
tions of the extremities, foot or hand, and impaired growth of nails. 

8. Thrombosis may occur in attacks with the following symptoms refer¬ 
able to the sudden closure of vessels; pain in the calf of the leg or foot, in¬ 
ability to walk, pallor of the forepart of the foot, coldness, blanching of the 
foot on elevation, loss of pulsation in the dorsalis pedis, posterior tibial or 
popliteal arteries, or all of these, sometimes followed by the development of 
trophic disturbances, and even gangrene, or at other times eventuating in 
more or less complete recovery. 


9 


130 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XXIII 

METHODS OF INVESTIGATION OF GANGRENE 

The identification of specific minute architectural peculiarities in 
thrombo-angiitis obliterans, the understandable and acceptable explana¬ 
tions therefor given elsewhere; 1 the gross and microscopic recognition of the 
atherosclerotic lesions, the demonstration of constant and immutable differ¬ 
ences between the thrombotic obturating changes in the blood vessels, 
and the hyperplastic endarteritic processes; all these have permitted us to 
correlate accurately a clinical, pathological and structural classification. 

On the other hand, the vasomotor and trophic neuroses, by reason of our 
imperfect knowledge of anatomic as well as functional derangements of the 
vegetative and sympathetic nervous systems, must be grouped principally 
upon a basis of clinical characteristics and similarities. 

Since a correct concept of the distinctive clinical features of certain vascu¬ 
lar lesions must needs depend upon repeated mental comparative association 
of the gross and minute visual findings obtainable from the vessels of ampu¬ 
tated limbs, with the anamnestic, subjective and the objective physical 
signs, it is advisable that the student have the opportunity of viewing as 
many pathological specimens as possible. Through these he should be 
able to supplement his routine observation with the anatomical comple¬ 
ment essential for thorough comprehension. Then, too, will the disassocia- 
tion of hydrostatic and mechanical factors from the attendant evanescent 
or transient neurotic symptoms be more readily understood; and then will 
the striking differences and peculiarities of symptomatology and clinical 
course in the vasomotor neuroses be better appreciated. 

In lieu of actual pathologic material intensive application to the study of 
the lesions described in other chapters may act as a good substitute. 

In consonance with the trend of modern medicine, which is not satisfied 
with barren labelling and dividing of morbid conditions into classes according 
to the presence or absence of certain qualities, we must endeavor to supple¬ 
ment clinical phenomena with a well-grounded and searching method 
of investigation such as will be herein described. It was through the results 
obtained by it and the hypotheses evoked by its application, that a satis¬ 
factory differentiaton of the neurotic and the physical symptomatology was 
made possible. 

For the sake of clearness and emphasis let us recapitulate by title what a 
correct method of approach should include 

(1) The general appearance of the limb 

(2) The presence or absence of rubor or cyanosis in the pendent position 
of the limb 

(3) The existence of ischemia on elevation of the limb and the Interde¬ 
pendence of change of position and blanching 

(4) The absence of some or all of the usual arterial pulsations 

(5) The angle of circulatory sufficiency 

(6) The possibility of eliciting reactionary or induced rubor 

(7) The presence of migrating phlebitis 

(8) The existence of trophic disorders and gangrene, and 

1 The author’s interpretation of the acute and chronic lesions in the vessels is given in 
detail in Chap. LXI-LXII. 


METHODS OF INVESTIGATION OF GANGRENE 


131 


9. The other refinements of physical diagnosis or special tests described 
elsewhere. 

Certain salient facts in connection with the distinguishment and classi¬ 
fication of the varied clinical morbid complexes here under discussion, deserve 
mention and careful consideration. Without the correct mental approach 
in our methods of differentiation, the confusion in diagnosis now so wide¬ 
spread will tend to become perpetuated. Let us then focus our attention 
on certain essentials that should be borne in mind. 

First, there are two distinct, clinically discrete and pathogenetically 
separable types of morbid process in the extremities, both associated with 
manifestations of circulatory derangement, exceedingly similar in many of their 
objective and subjective phenomena. These are the organic and the neuro¬ 
pathic affections of the blood vessels or vasomotor, or vasomotor and trophic 
disorders. 

Second, these two forms may be again subdivided into clinical entities 
some of which represent essentially diverse pathological lesions, others how¬ 
ever, corresponding in the present state of our knowledge, to different kinds of 
derangement in the vegetative and sympathetic nervous systems, the exact 
nature of which is unknown. 

Third, whereas the anatomic alterations in the vessels in the organic type 
of vascular disease have been satisfactorily classified by virtue of the recogni¬ 
tion of gross architectural and histological differences in the blood vessels, and 
whilst the causal relations between structural changes and symptomatic 
effects have been explained beyond question, such harmonious relatively 
has not been established between the characteristic phenomena of the vaso¬ 
motor affections and the nervous system where the motivating agency is 
supposed to reside. In the latter, theoretical assumptions alone are offered in 
the interpretation of the varied and bizarre manifestations, since microscopic 
and microchemical deviations from the normal have not been obtainable. 

Fourth, the organic types may be attended with vasomotor phenomena, 
but the latter do not justify the assumption of the coexistence of the two 
forms of disease. Some of the appearances imitate true vasomotor symp¬ 
toms, but are clinically dissimilar under the application of proper tests, and 
of wholly different origin. Others are veritable vasomotor manifestations, 
the expression of irritative and exhaustive influences in the sympathetic 
system, usually of transitory or even fugitive nature, surely of insufficient 
duration to be recognized as, or segregated into clinical or pathological 
entities. 

Fifth, the clinical phenomena attending organic vascular lesions of the 
extremities when manifested as rubor, ischemia, nutritional and circulatory 
disturbances—including atrophy, swelling, edema, trophic disorders and 
gangrene—may not be sufficiently characteristic to permit of precise differ¬ 
entiation from the true vasomotor affections. Even with additional sub¬ 
jective data, decision may not be possible. It is through an investigation of 
the circulatory functions in the affected limb in the manner previously de¬ 
scribed that pathognomonic signs may be obtained. The dictum to refrain 
from diagnostic conclusions based on anamnestic and visual information 
alone, is applicable here, and worthy of the strongest emphasis. Any 
scheme which has the identification of the various interrelated or even com¬ 
pletely diverse morbid entities in view, is inadequate and unsatisfactory 
unless the data obtainable through physical examination are accorded due 
weight and consideration. 


132 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Before proceeding to the discussion of the various forms of gangrene and 
to the symptomatology, pathology, diagnosis, and treatment of both organic 
and neurogenic morbid processes that result in, or threaten to bring about 
tissue death, it may be well to dwell more in detail on some of those salient 
phenomena upon which their advent is often foretold. These are pain, 
arterial pulsation, and “intermittent claudication . ” The other phenomena 
already alluded to, namely the coldness of the extremity, cyanosis, lividity, 
ischemia, rubor or erythromelia, trophic disorders, and thrombosis shall 
receive more comprehensive attention under each and every separate malady 
in which they may present themselves. 


CHAPTER XXIV 

DIAGNOSTIC SYMPTOMS—ARTERIAL PULSATION 

The detection of the presence of pulsation in the palpable arteries of the 
extremities, namely the ulnar, radial, brachial, dorsalis pedis, posterior tibial, 
popliteal and femoral—is one of the most valuable physical signs for the 
recognition and differentiation of a symptom-complex due to vascular disease 
or of vasomotor incitement. Whilst the pulse in the above mentioned arteries 
of the upper extremity can usually be elicited in the normal individual except 
aberrant radial and deep seated ulnar vessels, a number of extraneous con¬ 
ditions, seem to influence the demonstrability of the pulses in the lower limbs. 
Both an anomalous course as well as concealment through adiposity can 
invalidate the palpatory physical findings. 

The incidence of pulsation in the normal has been investigated by Erb’s 
assistants, who found that single pulses eluded detection, in somewhat less 
than i per cent of the 700 ward cases that he examined. In the author’s 
experience, tests of some 200 cases—that were regarded as normal, and in 
which the possibility of any excessive compromise of arterial integrity 
could be excluded—failed to evidence more than one instance of absence 
of the dorsalis pedis pulsation per cent). 

Therefore, the demonstration of palpable evidence of obliteration through 
the disappearance of pulse, is to be accorded great weight as a sign of organic 
vascular occlusion, particularly if elicited at a period free from possible 
vasomotor spastic phenomena and demonstrated repeatedly under varying 
circumstances. 

Fortuitous interference with the demonstrability of the arterial beat 
through changes in the skin, as edema, eczema, elephantiasis, adiposity, 
and other exceptional causes, must be given proper consideration. 

The popliteal pulse can be best felt in the following manner: With the 
patient prone and the leg flexed to the vertical and with muscles relaxed, the 
examining fingers enter the upper half of the popliteal space where the vessel 
can be readily discovered by pressure downward against the femur (Fig. 42). 
It is only in very stout individuals that pulsation fails to manifest itself in 
non-occluded arteries. 

Elsewhere will be discussed those occasional examples of vast functional 
exclusion of the arterial tree, where the femoral, popliteal, posterior tibial 
and dorsalis pedis pulsations are imperceptible, and in which arterial oblitera¬ 
tion of indeterminable nature is believed to exist. Enough clinical observa- 


DIAGNOSTIC SYMPTOMS—ARTERIAL PULSATION 


133 


tions are at hand to bear testimony to the view that embolic closure of some 
of the larger arteries of the extremities may take place with apparently no symp¬ 
toms, or such minimal ones as to completely escape the notice of the patient. 
This conclusion has been arrived at through the study of incipient clinical 
stages of embolic obturation of larger arteries in patients already under obser¬ 
vation for definitely proven embolic or thrombotic gangrene of another 
extremity. With the sudden advent of the signs of impaired circulation in a 
foot, or with a vague history of pain and coldness of abrupt onset, the 



absence of pulses and other phenomena makes the diagnosis clear. And 
still, by virtue of the developing collateral channels, all evidences of circu¬ 
latory disturbance may disappear except the absent pulses; and a clinically 
unrecognizable phase may then present itself to a future observer. For such, 
the clinician will have but the altered pulses and the accompanying mani¬ 
festations, if any, to guide him. The history of trouble in another territory 
may be an aid; but only a vague record, if any, in the limb now examined will 
be at his disposal. 

Two types have come under our observation. 

(1) Embolic closure of a large artery of the lower extremity, symptoms of 
imminent gangrene, rapid and adequate substitution of the collateral circu¬ 
lation, a latent or functionally cured stage, without trophic lesion being the 
issue. 

(2) Embolic closure of the posterior tibial artery above its bifurcation in 
cases of multiple emboli of the extremities, with an identical sequence. 

A more complete discussion of this subject will be found in Chap. LII. 

Whilst the absence of pulsation at the usual palpable sites may be regarded 
as indicative of arterial closure in most instances, the existence of pulsating 
vessels does not preclude vascular obturation in certain other territories. 
Both clinical observation and pathological examination of amputated limbs 
have conclusively shown that extensive closure of the plantar arteries and 
even the digital and dorsalis hallucis can exist, whilst the posterior tibial, 



134 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

dorsalis pedis and anterior tibal arteries pulsate strongly. Clinically too, the 
usual symptoms of thrombo-angiitis obliterans and even gangrene may be 
coincident with pulsating vessels, when the plantars alone are affected. As 
the disease progresses, both the posterior tibial and dorsalis pedis may become 

occluded. . . 

Many observations, clinical, operative and anatomic through dissections 
made by the author attest to the fact that arteries in which pulsation is usu¬ 
ally perceptible may fail to beat, although at the site of palpation their patency 
is conserved. Blood may trickle or flow through such channels without pulsa- 
tive effect on the vessel wall. So in a case of embolism of the brachial artery, 
in which arteriotomy and embolectomy were performed (Chap. LXXXV) the 
flow through the section beyond the obstacle could be readily demonstrated. 
Exceedingly interesting and conclusive evidence was also obtained in another 
case of embolectomy of the brachial artery, where, although an additional 
more remote territory was opened, by removal of the clot, the radial pulse 
remained abolished, not to return until 7 months after the occlusion. 

Absence of Pulsation Distal to Occlusive Thrombi—That the absence of 
pulsation does not always indicate organic occlusion, but may signify empty 
vessels distal to the occlusive embolus or thrombus, has been frequently 
observed in thrombo-angiitis obliterans and may also occur in cases 
of embolic gangrene of cardiac origin or in thrombosis complicating athero¬ 
sclerosis. It will be pointed out elsewhere how the return of circulation 
through collaterals demonstrates the patency of such seemingly closed vessels, 
and how this reappearance of pulse has often been misinterpreted as evidence 
of the beneficial results of treatment. 

Here it may be well to emphasize the occurrence of imperceptible pulses 
beyond the point of thrombotic occlusion in cases of atherosclerosis. As an 
example may be offered the following interesting case. 

J. R., male, aged 47, diabetic with advanced atherosclerosis; sudden advent of gangrene 
of the right foot and leg with absence of pulsation in the popliteal, femoral and external iliac 
arteries for a distance of about 1 inch above Poupart’s ligament. 

Amputation below the level of the origin of the profunda artery through the upper 
fourth of the thigh. At this level the femoral artery was partly closed by atherosclerosis, 
partly by recent thrombosis; almost no bleeding at this level, amputation being performed 
without a tourniquet or Esmarch. Five days after the operation a strong pulse could be 
felt in the femoral artery down to within about V 2 inch from the point of section, the wound 
having been left wide open. 

In explanation of the return of such a pulse, two theories can be advanced; 
one, that the occlusive thrombus in the external iliac was dislodged into the 
femoral just above the point of ablation, or that the common and upper super¬ 
ficial femoral had been patent; and that through establishment of the 
collateral paths the pulse became reestablished. The latter is in the author’s 
opinion the correct explanation, since the character of the thrombi and their 
age would preclude their having been detached after the amputation. 
Similar reestablishment of circulation is described elsewhere as occurring in 
the vessels of the upper extremity after embolic closure of the brachial 
artery. 


DIAGNOSTIC SYMPTOMS—PAIN 


135 


CHAPTER XXV 

DIAGNOSTIC SYMPTOMS—PAIN 

Pain is such a varied phenomenon both as regards its appearance, con¬ 
stancy, methods of excitation in the organic and neurogenic forms of arterial 
affection of the extremities, that it may be well to analyze its method of 
origin and some of the characteristics in the maladies in which gangrene may 
occur. 

In erythromelalgia , it is interesting to note that in the majority of the 
cases the pain does not follow the path of any of the peripheral nerves, nor is it 
encompassed within the territory or distribution of any nerve root. Further¬ 
more, in the quality of the pain there seems to be a difference here as 
contrasted with the common neuritic and neuralgic forms of pain. There is 
a deep-seated burning, poorly limited, constant, susceptible to exacerbations 
that is quite different from the pain described in the neuralgic cases. A 
similar condition is noted in cases of frozen extremities, when they suddenly 
enter into a warm room, the blood rapidly returning. This would arouse 
the suspicion that the pain is related to alterations in the vessels. 

Centripetal conducting elements of the sympathetic (Chap. IV) are 
numerous according to anatomical investigations. It would not be too auda¬ 
cious, therefore to believe that irritation of the centripetal fibers may evoke 
pain. If we accept the notion of the possibility of pain of sympathetic 
origin, we must seek a special form of irritant for the excitation of such pain. 
This is true, since in affections of the sympathetic nerve of the neck, 
excitation leads to mydriasis, and narrowing of the vessels without pain. 

We may assume that in certain arterial diseases , such as arteriosclerosis, 
irritation of the sympathetic plexus in the adventitia could cause stimuli 
that are transmitted or transferred in the spinal segments to sensory tracts, 
causing the so-called referred pain. But we cannot exclude the possibility 
that pain may be occasioned by alteration of the centripetal nerve fibers 
emanating from the blood vessels themselves, even though these under ordi¬ 
nary circumstances do not carry such impulses. 

In erythromelalgia it is possible that pain is occasioned by direct irritation 
of the sensory sympathetic elements in the vessel wall; for, the vasomotor 
and sensory symptoms often occur almost simultaneously in this condition. 

In thrombo-angiitis obliterans, the acute pain that is associated with the 
attacks described as the attacks of acute thrombo-angiitis obliterans, may also 
be, and probably is of the same origin. The vessels themselves become pain¬ 
ful. This pain is of a different nature from that which is associated with 
exercise (intermittent claudication) and that which precedes and attends the 
development of trophic lesions of the distal parts. Impulses along the 
usual sensory paths would account for the pain accompanying ulcers, fissures, 
and gangrene; but even here the abnormal intensity of the sensory impressions 
would lead one to believe that a distinct alteration in the threshold for pain 
often exists. 

In Raynaud’s disease sensory phenomena, be they anesthesia, hyperaes- 
thesia or pain, do not correspond to the territory of a single nerve, but extend 
rather diffusely over the extremity, being rather confined to the area in which 
there are vasomotor and trophic disturbances. The difference noted is that 
the pain is apt to extend farther proximally, and radiates to a greater degree 


136 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


towards the root of the extremity. The absence of relation between its 
situation and the course of distinct nerves, the diffuse distribution, the 
simultaneous occurrence of pain in both extremities, and its extension into 
the deeper tissue, these are facts that speak for a more central lesion. Be¬ 
cause of the return to normal in certain cases, and the transitory nature of 
the symptoms, Cassirer concludes that in the Raynaud complex there may 
be lesions that are easily repaired, possibly superinduced by vasomotor 
influences and their consequent trophic effects. This assumption, however, 
could only be extended over a limited number of cases. 

In most of the cases of true Raynaud’s disease an exact localization of 
the lesions cannot be made. The nature of the pain and its distinct rela¬ 
tionship to vasomotor phenomena point to a very evident association with 
the vasosensory fibers. 

In organic obstructive arterial diseases various explanations may be given 
for the relationship between the advent of pain and its intensity to the position 
of the limb. It is usual (though not without exception) to find that pain will 
be evoked whenever the limb is elevated sufficiently long to produce a very 
marked ischemia, or at least, if this position be maintained over a sufficient 
period of time. It is impossible to assert just how important is the ischemia 
itself, with its power to cause irritation of the sensory nerves, and to what 
extent the secondary reflex or direct spasm of the vessels is an exciting moment. 
Doubtless both agencies may play a role. 

Paroxysmal pain of a diffuse variety is occasionally severe; it may come on 
in insufferable nocturnal attacks, especially in those arteriosclerotic cases in 
which recent thrombosis has been superadded. No satisfactory explanation 
for this manifestation has as yet been presented. Possibly it results from a 
summation of the excitant action of cumulative chemical effects, or of pro¬ 
longed circulatory stasis. The latter would be favored by inactivity during 
resting (sleeping) periods, and might attain a climax sufficient to incite spasm 
in still non-sclerotic smaller arteries (discussed more fully in Chap. XXVI). 

This phenomenon would be analogous to that of intermittent claudica¬ 
tion, but of different causation—a paradoxical intermittent claudication 
of inactivity. 

The pain induced by prolonged pendency of the limb, particularly if this 
position be preceded by a period of elevation, is perhaps more difficult to 
account for. It is not uncommon to find patients who are unable to allow the 
legs to hang down for a protracted period, particularly if well marked rubor 
and trophic ulcers or fissures be associated phenomena. Here, we may pre¬ 
suppose inadequate oxygenation of the blood as evidenced by the ensuing 
lividity when the posture is continued. The manifestations do not seem to 
be unlike those that are expressed by tingling, formication and pain in the 
fingers of a person who had exposed them to excessive cold; or in whom a con¬ 
stricting (Esmarch) bandage had been applied and released. In such a case 
the effects of ischemia and subsequent hyperemia or even stasis, cause 
responses in the sensory nerves. Or, perhaps, even the vascular channels, 
themselves are the source of sympathetic sensory impulses. In the present 
state of our knowledge we must be content to attribute to both the inherent 
vascular nervous paths and also to the sensory nerves a role in the incitement 
of the above types of pain sensation. 1 

The alteration of tonus (change in threshold) in the spinal cord that may 
be produced by persistent pain and its influence on vasomotor stability are 

1 A more detailed statistical and clinical description may be found under the Chapters on 
Thrombo-angiitis obliterans. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 137 


discussed elsewhere. 1 It is not infrequently stated that the distress is 
especially intense at night. This may be in part due to variation to threshold 
for pain perception; but it is in part referable to the lack of motion and 
resulting stasis. 

-''The pain associated with trophic disorders , such as ulcers over the distal 
parts of the phalanges, may be exceedingly intense and quite out of propor¬ 
tion to that which we would expect from lesions of similar nature and extent 
complicating other affections. It is apt to be noteworthy in its degree in 
thrombo-angiitis obliterans, and may be so excruciating as to render the 
patient neurotic and to beg for amputation of a toe or even of the leg/ The 
threshold for the pain sense is indubitably altered in these cases, and a con¬ 
dition of hyper excitability of the sensory domain probably exists. Indeed, 
persistence of pain of similar nature may continue for days or weeks after 
amputation of the limb. 2 On the other hand, it is reported that injection 
of absolute alcohol into the posterior tibial nerve may completely abolish 
pain attending trophic ulcers of the foot. Whilst no doubt is cast on the 
correctness of such observations, it is difficult to reconcile this therapeutic 
effect with the above statement of the persistence of pain after amputation. 


CHAPTER XXVI 

DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 

Thoroughly intrenched in medical parlance, this term, though giving rise 
to much confusion, may still be retained, if its import, limitations, and exact 
significance be comprehended. Suggested by Erb as applicable to a dis¬ 
tinctive clinical picture, it has by virtue of incorrect interpretation, been 
transferred to a multitude of affections, the true nature of which has oft been 
unrecognized, and has been confounded with Raynaud’s disease. Although 
believed by some to denote morbid entity, it should more properly be confined 
and restricted, as a designation for a complex of symptoms , such as may be asso¬ 
ciated with a number of different pathological processes, or even vasomotor 
affections. In this sense, not indicative of any particular disease, but as a 
composite of manifestations, it will be used by the author. That there may 
be an association of other manifestations of vasomotor neuroses or that it may 
itself be of neurogenic origin cannot be denied. Nevertheless, much progress 
will be made in the differentiation of vascular affections of organic from those 
of neurogenic derivation, if the limitations above suggested be adhered to. 

SYMPTOMS 

The characteristics of the Erb type of intermittent claudication are 
complete or almost complete absence of pain or discomfort in a limb when at 
rest, commencement of disturbances, pain, tension, paresthesiae, weakness 
shortly after walking is begun, gradual intensification of these until walking 
is embarrassed and finally impossible, and the disappearance of the disorders 

1 See page 42 . 


138 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

after a period of rest. Objectively there may be coldness, cyanosis, transi¬ 
tory patches of rubor interspersed with the cyanosis, with a marmorated 
appearance of the skin. At times cadaveric ischemia is noted: one or more 
arteries of the foot usually fail to pulsate. Trophic disorders such as dry 
skin, ungual dystrophies and gangrene may complicate the picture. 

This is the symptom-complex as it is associated with organic vascular 
disease in contradistinction to the angiospastic or functional variety that is 
to be grouped with the vasomotor neuroses. This description of a symptom- 
complex is incorrectly extended to include a number of diverse infections. 

Intermittent claudication may be described as a manifestation accompany¬ 
ing two totally diverse processes: 

(1) Vasomotor neuroses (angiospastic neurosis); and 

(2) Obstructive arterial disease (arteriosclerosis, thrombo-angiitis oblit¬ 
erans, etc.) r , f 

Oppenheim 1 distinguishes a (1) benign and (2) malignant form, the former 
a functional or purely angiospastic phenomenon, the latter associated with 
diseased arteries 

I. The Vasomotor Type. —A concomitant neurosis of the neuropathic 
diathesis, is said to coexist with intact arteries and to depend on spasm of the 
arterial wall. Oppenheim mentions the following characteristic instance in 
which transitory pain on walking with disappearance of pulse, coldness and 
blueness of the toes were significant. 

A male thirty years of age had been suffering for two years from painful sensations in the 
feet on walking, these becoming gradually more severe so that at time cramps and numbness 
in the feet and legs were pronounced even after fifty paces. After walking two hundred 
steps in the office, painful fatigue with coldness of the skin and bluish discoloration set in, 
together with a disappearance of both dorsalis pedes pulses (?). After a rest of a minute, 
the right dorsalis pedis pulse was again perceptible. Several years later, all the symptoms 
had disappeared, and the arteries of the foot were distinctly discernible. 

Another case quoted by the same author is equally valuable. 

Miss S., 22 years of age had frequent attacks of local syncope in her finger since her 
sixteenth birthday. In the winter of 1898 there was much emotional strain, and in the 
early summer of the same year she took a long and arduous tramp. Immediately after this, 
the following condition developed. After walking 100 to 200 steps she experienced severe 
pain and coldness in the left leg, and to a lesser degree in the right; the calf of the leg seemed 
to become stiff and there were pricking and stinging sensations. After standing still for a 
few minutes, she could go on again for a short time. The patient was a slender, anemic 
individual. The pedal pulses were present though weak. When the patient was allowed 
to walk around the room some 15 to 20 times, the foot became pale and bluish, and the dorsalis 
pedis pulse was no longer perceptible. Five to 10 minutes later the beat returned. 

These forms may have to be differentiated at times from Raynaud’s 
syndrome and erythromelalgia. When the angiospastic phenomena affect 
not only the territory of the muscles but implicate the cutaneous arteries, 
vasomotor manifestations in the integument appear that may mimic the 
above conditions. 

The points valuable in differentiation are: In intermittent claudication, 
the dependence on motion is characteristic even though the picture is ob¬ 
scured by evidences of vasomotor irritation (blanching, cyanosis and reactive 
rubor), and the temporary or permanent absence (?) of pulses; in Raynaud’s, 
the spontaneous, symmetrical and paroxsymal appearance with patent arteries 
is the rule. 

Whilst the careful observations of eminent authorities on the occurrence 
of the angiospastic, functional or vasomotor type of intermittent claudication 
deserved respectful consideration, a study of a large number of cases of 
1 Oppenheim, Deutsch. Ztschr. f. Nerven., XLI, p. 376. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 139 


organic disease of the vessels of the lower extremity, has convinced the author 
that the incipient stages of true vascular obliteration when accompanied by similar 
symptoms is frequently overlooked , and interpreted as a vasomotor affection. 

II. The type accompanying organic vascular disease is seen in athero-, 
arteriosclerotic and syphilitic affections as well as in thrombo-angiitis 
obliterans. Here the attendant vasomotor phenomena must not be regarded 
—as Erb would have it—as integral elements of the syndrome, intermittent 
claudication, but as irritative manifestations, frequently due to external 
thermal influences, emotions or other excitants. The associated vasomotor 
symptoms should not be regarded as part of the Erb complex , since they are 
present even when the symptoms of intermittent claudication are wholly absent. 
The grouping of vasomotor signs with the spasmodic and sensory phe¬ 
nomena of Erb, is insufficiently warranted, therefore, and it is for this 
reason that the author shall merely include the sensory symptoms in the 
designation “intermittent claudication.” Cases of organic vascular dis¬ 
ease, such as thrombo-angiitis obliterans, therefore, may present vasomotor 
phenomena, side by side with these regarded as “intermittent claudication.” 

HISTORICAL 

Keeping in mind that many authors have described intermittent claudication as a 
morbid syndrome of varied pathogenesis, 1 it may be well and of historical interest to recount 
some of their observations. 

In 1858 Charcot described a clinical picture typical of intermittent claudication. A 
male 54 years of age complained of weakness, numbness, cramps and stiffness in his right 
leg after walking for about one quarter of an hour. After a pause of some 5 to 10 minutes, 
walking would again call forth the symptoms. 

The relationship between these manifestations and similar occurrences in animals 
previously described by veterinarians, was noted and commented upon by Charcot at 
that time. 

Erb gave a classical and extremely illuminating description of the symptoms in the year 
1892. A number of different designations and appellations had been employed by various 
authors, amongst which may be mentioned the following: 

Charcot 2 described a Claudication intermittente par obliteration arterielle; and also, 
Paralysie douloureuse ischemique. Erb 3 suggested Dysbasia intermittens arteriosclerotica; 
Higier, 4 Angiosklerotische paroxysmale Myasthenie; Oppenheim, 5 Dysbasia angiosclerotica; 
Walton 6 and Paul, Angina cruris. Grossman, 7 Angioscklerotische intermittierende Muskel 
Parese; and Determann, 8 Akinesia or Dyskinesia intermittens angiosclerotica. 

Charcot had previously called attention to an affection in horses that had its analogy in 
the human, and to which he assigned the term “Intermittent Claudication.” Boullay 9 
had noted—as had also other authors, subsequently (Rademacher, 10 Bother, 11 Votsch, 12 
Sommer 13 and Goubaux 14 ) that an ischemic condition of the hind legs regularly appeared as 
a causal or concomitant phenomenon, so that it was a priori clinically acceptable to surmise 
that impaired circulation could also account for similar symptoms involving the muscles of 
locomotion in the human. 

1 Erb, Deutsch. Ztschr. f. Nervenh., 13, 1898, 76. 

2 Charcot, Compt. rend. Soc. de Biol., 2, Serie 12, 1858, p. 225. 

3 Loc. cit. 

4 Higier, Deutsch. Ztschr. f. Nervenh., 19, 1901, S. 438; Neurol. Zentralbl., 1910, 911. 

5 Oppenheim, Deutsch. Ztschr. f. Nervenh., 17, 1900, S. 317; Deutsch. Ztschr. f. 
Nervenh. 41, S. 376. 

6 Walton, Boston Med. and Surg. Jour., 146, 1902, p. 351. 

7 Grossman, Deutsch. Arch. f. klin. Med., 66, S. 500. 

8 Determann, Deutsch. Ztschr. f. Nervenh., 24, 1905, p. 152. 

9 Boullay, Ac. roy. de Med. Seance du n Oct., 1831. Arch. gen. de Med., 1831, 

XXVII, p. 425. 

10 Rademacher, Gwilt u. Hertwig’s Magazin f. d. ges. Tierheilk., 1838, IV, S. 455. 

11 Bother, Ztschr. f. d. ges. Tierheilk., 1839, VI, S. 425. 

12 Votsch, Herings Repertorium d. Tierheilk., 1839, VI, S. 425. 

13 Sommer, Gwilt u. Hertwig’s Magaz. f. d. ges. Tierheilk., 1843, IX, S. 464. 

14 Goubaux, Recueil de Med. Vet. prat., 1846, XXIII, p. 578. 


140 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In the so-called “Boiterie intermittent des chevaux”, (intermittent limping of horses) 
one may observe that an affected horse presenting no symptoms at rest or when going at a 
slow pace, will, after five to fifteen minutes of hastened gait or trot, drag one or the other 
hind leg. Even a short run may cause it to perspire, and to turn its head in the direction 
of the hind quarters. Its expression becomes anxious and breathing is accelerated. In 
short, all the signs of pain, and weakness in the limping extremity become evident. The 
affected limb becomes simultaneously cold and pulseless. If the horse be now driven still 
further, the functional enfeeblement may increase to such an extent, that the horse breaks 
down completely, lying helpless and paralyzed. After a pause or rest of five to thirty 
minutes it becomes wholly restored and capable of assuming normal pace. Since such 
attacks recur whenever the animal moves at a moderately rapid gait, the horse becomes 
practically useless. . .... 

Autopsies have revealed an obliteration of the distal portion of the aorta in the bilateral 
cases, and closure of the iliac or femoral artery in unilateral, when one limb alone is involved. 
Gangrene does not occur because of the relatively favorable conditions that obtain for the 
establishment of a collateral circulation. 

In Charcot’s first and analogous case an aneurysm of the right iliac artery with oblitera¬ 
tion of the distal portion of the artery was present. This aneurysm and consecutive 
thrombosis had followed a bullet injury sustained some twenty-one years previously. 

Curiously enough this first reported and clinically observed case of intermittent claudi¬ 
cation in a human being had for its anatomical basis a most uncommon lesion, since, as 
subsequent investigation revealed, symptoms of intermittent claudication usually accom¬ 
pany and are due to disease of the peripheral vessels of an extremity (Erb). 

CLINICAL TYPES 

Although the organic vascular form of intermittent claudication seems 
to be the most common, the literature abounds in clinical examples warrant¬ 
ing the recognition of additional types. We may summarize. 

I. Charcot—Erb’s variety (Dysbasia angiosclerotica intermittens). 

II. The functional vasomotor type (Oppenheim). 

III. Intermittent claudication in other territories. 

IV. Acute forms (so-called) probably thrombo-angiitis obliterans, or 

V. Apokamnosis or artificially induced intermittent claudication. 

I. Dysbasia Angiosclerotica Intermittens 

This type (according to the literature), includes the typical symptoms 
associated with diseased arteries and has been variously called, claudication 
intermittente par obliteration arterielle (Charcot). Paralysis douleureuse 
ischemique (Charcot), angiosklerotische paroxysmale Myasthenia (Higier), 
angiosklerotische intermittierende Muskelparese (Grossmann), and Angina 
cruris (Walton). 

Whilst the symptom-complexes here described are alluded to by most 
authorities as indicative of a morbid condition of which they are the most 
important manifestations, the author wishes to emphasize in advance that 
he cannot subscribe to such a view. For he will show that intermittent 
claudication is more correctly merely a designation for a group of associated 
phenomena that may be evoked by a number of varied and diverse patholog¬ 
ical conditions. Nevertheless, for a thorough comprehension of the subject it 
may be well to give a brief review of the symptomatology, etiological factors, 
clinical course and pathology, as they have been set forth by other authors. 

Oppenheim and Cassirer 1 describe the following picture. The manifes¬ 
tations begin slowly as a rule, affecting both lower extremities simultaneously, 
or successively one and then the other after varying intervals in different 

1 Cassirer, Loc. cit. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 141 


cases. First, there appear sensory symptoms such as disagreeable sensations 
in the foot, toes, soles, and calf of the leg with paresthesia, or with a feeling 
of coldness, alternating possibly with burning sensations, sensory symptoms 
in the foot or calf of the leg—all of these, or a combination of several develop¬ 
ing after walking, and disappearing after repose. Vasomotor symptoms are 
frequently associated at the very onset of the symptoms, the patient noticing 
that the feet become blue and cold, sometimes strikingly cyanotic after walk¬ 
ing, or when allowed to remain in the pendent position for some time. Such 
discoloration may alternate or be associated with areas of redness, or the toes 
may become ischemic. These vasomotor phenomena also are apt to be 
intensified or appear only after locomotion. 

Cassirer remarks that as the pain and cramp-like sensations increase, 
the muscular disturbances become intensified, so that the patient can walk 
only with difficulty. In this stage frequent rests become necessary, and 
finally walking may have to be given up altogether until the symptoms have 
wholly abated. Such recovery after rest comes on after several minutes, 
when a continuance of locomotion is resumed with the greatest difficulty. 
There may be considerable variations in the degree of suffering and func¬ 
tional interference. 

Subjective manifestations of vasomotor nature were noted in 25 out of 36 
cases. As a rule there was a feeling of coldness whilst more rarely the oppo¬ 
site condition obtained. Local ischemia particularly over the plantar aspect 
of the feet could be evoked by permitting the patient to walk rapidly around 
the room, when sensory and motor derangements could also be elicited. 

Goldflam 1 states that some of the latent cases of intermittent claudica¬ 
tion can be recognized by noting the onset of vasomotor symptoms after 
exercising the feet and legs. Thus he describes changes in the color of the 
feet, blanching, disappearance of the small veins with collapse of the veins. 
In the advanced cases the feet and lower legs may present a spotted cyanotic 
appearance with possibly hyperemic areas between the patches of cyanosis, 
the skin temperature usually subnormal, rarely elevated. 

Erb, Cassirer and others speak of the absence of the dorsalis pedis and pos¬ 
terior tibial pulses as the most important objective signs. In most of the bilat¬ 
eral cases all four pulses of the feet are wont to be missing. 

In the clinical picture above described, it is remarked by a number of 
authors, that symptoms other than those mentioned are generally absent. 
The reflexes are usually normal, objective sensory disturbances do not occur 
and there are no neurologic findings. However, certain trophic disturbances 
of the skin of the feet may be noticeable, such as dystrophy of the nails and 
ulcers. Very frequently a decided degree of arteriosclerosis can be detected. 

Two facts stand out prominently as having a causal relationship with the 
symptom-complex: first , certain circulatory and vasomotor phenomena; and 
second, the absence of the pedal and crural pulses. 

The circulatory and vasomotor phenomena that usually precede the 
manifestations of intermittent claudication and may be given the importance 
of prodromal signs, are described as attacks of peculiar paresthesiae (feel¬ 
ings of heat and cold, formication and sensation of “falling asleep”) with 
cyanotic, livid, marmorated or cadaveric discoloration of the foot and 
leg. The same interdependence of symptoms and locomotion, as noted with 
intermittent claudication obtains in the production of these visible signs. 
When the well marked motor disturbances of intermittent claudication are 


1 Goldflam, Neurol. Centralbl., 1910, S. 1. 


142 


CIRCULATORY AFFECTIONS OF TIIE EXTREMITIES 


fully developed, such objective and subjective paroxysms as here given may 
appear simultaneously. 

Coldness, cyanosis and pallor of the affected parts are noticeable when the 
patient complains of numbness or strange feelings in the toes. 

Erb called attention to the fact that in the well developed cases the feet 
are apt to show abnormalities in appearance, even with the absence of par¬ 
oxysms, that is, during the free intervals. When the extremities are allowed 
to hang down, they are apt to be cold, cyanotic, swollen. The skin is said to 
be abnormally dry, and the growth of the nails impaired. Bright red spots 
may be interspersed with the cyanotic areas, lending a marble-like appear¬ 
ance to the skin. Or, anemic areas may appear usually involving one or 
more toes, the feet becoming cadaveric and cold for varying periods of time, 
these phenomena being associated with prickling or sticking sensation when 
the normal redness or cyanosis returns. All these manifestations may be 
absent when the patient is at rest in bed, or in a warm temperature. All 
of these appearances , we believe , may belong to any of the types of organic arterial 
disease , and cannot , therefore be regarded as a separate entity. 

Examination of the Pedal and Crural Arteries.- —This may be regarded as 
of pathognomonic value in the diagnosis of dysbasia, angiosclerotic inter¬ 
mittens. The absence of pulses in one or more of the four pedal arteries is 
almost a regular finding, and may be accompanied by demonstrable thicken¬ 
ing and tortuosity of the vessel. Thus Erb reports that of 30 bilateral cases 
there was an absence of the beat in all four arteries in 16 cases; three in 2 cases 
and in 1 case absence of one pulse. All four pulses were palpable in but 4 
cases, and in these they were weak, three of the patients having evidenced 
thickening and sinuous vessels. Of 16 unilateral cases absent pedal arteries 
were noted in 13. 

Almost as important according to the above author is the examination of the popliteal 
and femoral arteries which often give positive findings, such as absent beat, or the above- 
mentioned organic changes. In the case of Bourgeois 1 there was an aneurysm of the 
popliteal artery. Simon 2 recorded similar symptoms in a case of embolus of the anterior 
tibial artery. Although a number of observations definitely offer conclusive proof that 
localized arterial disease such as aneurysm, embolism, etc. can also cause the symptoms of 
intermittent claudication, as a rule a more diffuse impairment of the circulation as produced 
by obstructive diseases of the peripheral arteries of the lower extremities is present. 

Clinical Course. —A perusal of the literature convinces one of the fact that 
a progressive and obliterating arterial infection is usually present. Striking 
also is the circumstance that spontaneous gangrene of the affected extremity 
is so frequently the issue. In the cases that are not treated, or in those which 
were refractory to all measures, there was described a progressive aggravation 
of the condition, or periodic recurrences with increasing intensity of symp¬ 
toms, finally eventuating in almost complete abolition of locomotion. With 
increasing intensity of the degree of circulatory disturbance and the con¬ 
comitant symptoms, gangrene of the toes of the foot, with proximal 
extension, is said to occur. 

II. Functional Vasomotor Type (Oppenheim) 

Nothnagel 3 recorded the following symptom-complex in a patient in 
whom the arterial circulation of one arm was impaired by reason of thrombo¬ 
sis of one of the axillary arteries. 

1 Bourgeois, F., These de Paris, 1897. 

2 Simon, Deutsch. med. Wchnschr., 1905, 19 , p. 754. 

3 Nothnagel, Berl. klin. Wchnschr., 1867, No. 51, p. 536. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 143 


A girl of twenty-five years was afflicted with striking fatigue, weakness, with pain and 
paresthesiae in the fingers and hand on doing but the lightest of work, all symptoms 
disappearing after a rest. 

Such observations confirm the assumption that any occlusive process in 
the arteries may serve as the basis for the manifestations of intermittent 
claudication. Therefore, not only the extremities, but other territories 
should offer clinical evidences of corresponding symptoms. 

Doubtless many of the cases of so-called vasomotor or angiospastic forms 
of intermittent claudication belong more properly to the vasomotor neuroses , 
intermittent claudication being only one of the manifestations, just as are 
cyanosis, ischemia and other phenomena. That Oppenheim 1 had been 
compelled to take this view and to renounce, in part, the classification of 
intermittent claudication previously suggested, was due to the publication 
of cases that were quite different from the classical forms of intermittent 
claudication, except for some of the motor and sensory symptoms. 

Thus, Westphal 2 called attention to spastic phenomena in the vessels of 
the lower extremity with disappearance of the anterior tibial and posterior 
tibial pulses during the attacks, (coincident with disturbances in locomotion) 
—in a case of hysterical pseudotetanus—a complex which surely cannot be 
classed with intermittent claudication, but which, because of the wide and 
indiscriminate application of this term, had been considered as another 
variety. 

In a woman with symptoms of pseudotetanus, there were associated attacks of vaso¬ 
motor manifestations involving the upper as well as lower extremities. At the beginning 
of a paroxysm, there was a pricking sensation in the fingers or the toes, gradually increasing 
in intensity to actual pain. At times the whole of the hands and feet would be involved, or 
but parts of these, either on one side or symmetrically. The affected regions would become 
cyanotic, or violaceous in color, or sometimes ischemic, pale and cold. Pallor would 
occasionally give way to cyanosis, and a deep prick with a needle could not entice a drop of 
blood to the surface. Variations in color would be manifold in distribution of time of 
appearance and duration. 

Most striking was the disappearance of the pedal beats during such attacks, whilst 
during the free intervals the feet were found normal, both as to color and as to the intensity 
of the arterial pulsations. The radial pulses, however, were always present. 

With the advent of these vasomotor phenomena, disturbances in locomotion were also 
noted. The patient would complain some time before the beginning of an attack of fatigue 
on walking and paresthesiae in the feet. With the actual onset of the attack, walking would 
become impossible. 

What an exquisite example of a pure vasomotor neurosis and how futile 
to force a clinical relationship between this disease and ‘‘intermittent claudi¬ 
cation!’’ That some of the cases described as intermittent claudication were 
said to have had evidences of an angiospasm in the pedal arteries, cannot be 
denied; but that the case of Westphal has any clinical or pathological affilia¬ 
tion with either the so-called organic or the functional types of intermittent 
claudication, is to be doubted. 

Record of an instance that was said to be due to toxic factors is that of a 
young man, in whom the symptoms of intermittent claudication seemed to 
depend upon psychic or emotional states (Schlesinger 3 ). The symptoms 
disappeared after one and a half years, only to return eight years later. 

Perhaps the most convincing example of the neurotic type of intermittent 
claudication is a case in which symptoms of this disease were associated with 

1 Oppenheim, Deutsch. Ztschr. f. Nervenh., 1900, Bd. XVII. 

2 Westphal, Berl. klin. Wchnschr., Dec. 9, 1907, XLIV, p. 1567. 

3 Schlesinger, Deutsch. Ztschr. f. Nervenh., Bd. 41, p. 235. 


144 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

the Raynaud phenomenon. The following description and case report will 
elucidate. 

Angioneurotic Intermittent Claudication with Raynaud’s Disease of_the Fingers.-— 

An example of so-called neurotic intermittent claudication is described (Rulf ), in which 
there were combined Raynaud’s disease of the fingers, intermittent claudication of the 
lower extremities, rubor of the tip of the nose and symptoms of migraine. . 

A woman 30 years of age, always of nervous temperament, began 6 years previously 

with severe attacks of migraine. , ... Aan A 

For the past 2 years the tips of the fingers would become numb and white as it dead. 
Rubbing or motion would restore the circulation. At first the fourth and fifth fingers were 
involved, later the others. For about 3 months the attacks of syncope were followed by 
asphyxia. The severity of the symptoms has been increasing; recently have been appearing 

several times weekly. , , . ,. ... 

The symptoms referable to the lower extremities antedated those of the upper slightly. 
There have been associated cardiac symptoms, in that attacks of weakness, reeling of 
faintness and prostration come on after walking. Recently pain has developed in the left 
leg after walking, necessitating frequent periods of rest. After a short walk, a feeling of 
tiredness appears in the left sacral region, the weakness and tiredness advancing so as to 
implicate the left thigh, knee and upper part of the leg. If the body were supported by 
the right limb, the left leg seemed warm again, and the symptoms would disappear. 

The dorsalis pedis and posterior tibial arteries could be found pulsating, but were diffi¬ 
cult to find” (?). The radials arteries were abnormally small. 

The temperature was found reduced over the left leg and foot, but not always, usually 
only after walking. The blood pressure was 115 systolic. 

This case is described as one of intermittent spasm of the vascular capil¬ 
laries , since the pedal pulses were neither diminished nor abolished during 
the attacks. The diminution of temperature over the left lower extremity is 
attributed to vasoconstrictor action. 

Curschmann, 2 also, accepts the possibility of an intermittent claudication 
with apparently intact (?) arteries, where the symptoms are referable to a 
genuine constriction of the pedal arteries. In two females (between the 
ages of 19 and 22) he found the typical manifestations associated with absence 
of the pulses of the feet and without any evidence of arteriosclerosis.. He 
claims that such instances are analogous to the intermittent asphyxia of 
the hands, differing in that the pulses are permanently absent in the former. 

It is, however, just this constant lack of beat in the pedal vessels that 
throws considerable doubt on the accuracy of his observations. A permanent 
arterial spasm is so foreign to analogous conditions elsewhere, that our mental 
approach to such a possibility can hardly divest itself of the suspicion that a 
true organic obliteration did exist. 

Relation of Angiospasm to the Organic Type of Intermittent Claudication. 

-—We have purposely retained here the designations, angiospastic (neurogenic 
or vasomotor) and organic intermittent claudication (dysbasia angiosclerotica 
—Erb), in order to express more clearly the views of the authorities who have 
employed these terms. For it must be borne in mind that amongst a large 
number of the continental observers, the conception of the malady “inter¬ 
mittent claudication” had taken root so strongly, that, with the discovery of 
diverse, contradictory and inconsistent physical findings, in arteriosclerotic 
arteries (Erb), in acute arteritis (Higier), in obstructed arteries (Higier), and 
with patent arteries (Oppenheim’s angiospastic form), a confusing collection of 
clinical descriptions had found their way into the literature. To clarify some 
of these notions, reference must be made to theories according to which vaso¬ 
motor neuroses are regarded not only as the antecedents, but also as actual 
harbingers of organic vascular changes in a causal sense. 

1 Rulf, Arch. f. Psychiat., 56, H. 1, p. 899. 

2 Munchen. med. Wchnschr., 1907, No. 51, p. 2522. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 

Oppenheim entertains the belief that the angiospastic neurosis with symp¬ 
toms of intermittent claudication may be a prodromal stage of what he terms 
organic intermittent claudication or “ dysbasia angiosclerotica. ” In defense 
of this proposition he cites a case of a young man in whom vasomotor mani¬ 
festations preceded by years, the final appearance of intermittent claudication 
with evidences of arterial obliteration. 

H. H., male, 28 years, gave a history of neuropathic tendency, insomnia, frequent 
attacks of “dead fingers,” and even local syncope in these, with sensation of “pulsations” 
in various parts of the body, with excessive sexual irritability. The feet showed nothing 
abnormal (February, 1895). 

Two years previously after emotion, he had pain with coldness in the calf of the legs on 
walking 1 to 3 minutes, necessitating a pause before further progression was possible. 
After lasting about a year, these symptoms disappeared. 

In 1899, a recurrence of difficulty in walking, with the right leg especially affected, was 
noted. The plantar aspect of the toes of this limb would become pale with slight cyanosis 
after fatigue. The corresponding dorsalis pedis artery could not be felt pulsating. 

In 1911 the pulses of the right foot were altogether absent, present on the left. Cold¬ 
ness and cyanosis were also striking signs. Pain and cyanosis appeared after walking 
30 to 40 steps. X-ray examination showed distinct calcification. 

In short, evidence has been brought forth, at least in this case, that the 
phenomena of intermittent claudication may coexist with pulsating vessels in 
a neurotic individual with other stigmata of a labile vasomotor system; that, 
later, such a patient may, after free intervals, pass over into a stage in which 
the peripheral arteries are arteriosclerotic and obturated. While such a 
chronological sequence of events doubtlessly may occur, the causal relation¬ 
ship between the stage of angiospasm and the subsequent development of 
organic disease, be this arteriosclerosis, thrombo-angitis obliterans, or throm¬ 
bosis, is not so clear. To conceive of peripheral thromboses as a compli¬ 
cation during the history of repeated attacks of vasomotor constriction, is 
logically permissible, and, certain observations of the author would support 
such an assumption. An analogous condition obtains in cases of gangrene 
in anatomically normal arteries and in the cases of thromboses in peripheral 
arteries without arteriosclerosis or other disease. 1 In some of these acro¬ 
cyanosis had been noted although intermittent claudication was usually absent. 

But to assume, as does Oppenheim, that there is an intimate motivating 
dependency between a prior neurotic status and a succeeding arterial disease, 
would appear an audacious hypothesis, in light of the fact that in that most 
intense and exquisite form of angiospastic condition , Raynaud’s disease , such an 
organic vascular eventuality is altogether lacking. 

A perplexing situation, diagnostically speaking, will not infrequently 
confront us, one that may be interpreted as reliable testimony in favor of 
Oppenheim’s belief. This is the circumstance that marked vasomotor 
symptoms, occasionally with, but usually without intermittent claudication 
may occupy the clinical picture, weeks, months, or almost years before the 
typical objective manifestations of thrombo-angiitis obliterans are recog¬ 
nizable. References to this type will be made in Chap. LIX. 2 To deduce 
a causal association between the excessive lability of the vasomotor func¬ 
tions and the consequent inflammatory and obstructive vascular lesions, 
would, in our opinion be unwarranted. 

Whenever pronounced neurotic vascular symptoms participate in the early 
stages of an insidiously developing organic obstructive arterial lesion, we 
must consider the following possibilities. 

1 See Chap. XCVIII. 

2 See Vasomotor Symptoms in Thrombo-angiitis Obliterans of the Upper Extremities, 
and also Chap. “Borderline Cases” CIV. 

10 



146 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


First, two independent diseases may overlap, coexist or follow each other. 

Second, minimal unrecognizable peripheral vascular obturating processes 
(as in thrombo-angiitis obliterans of the plantar arteries or peripheral pedal 
vessels) are present for a long time, and are a factor, not only in evoking the 
cyanosis or pallor of the digits on exertion, but also secondarily elicit a super¬ 
abundant quota of vasomotor response; and this, either by virtue of the super¬ 
fluity of waste products (toxins, C 0 2 , etc.) developed in poorly nourished 
territories, or by a relative ischemia when the circulation is impaired. 

Third, thromboses of the popliteal artery of clinically unobserved, 
stealthy advent, with adequately dilated collateral paths filling the dorsalis 
pedis and posterior tibial arteries may be accountable for a complex that is 
wont to be diagnosticated as a vasomotor form of intermittent claudication. 

A more complete exposition and an analysis of this subject are given in the 
section on the critique of so-called angiospastic forms of intermittent claudi¬ 
cation also in Chap. CIV. 

While Oppenheim lays great stress on two factors, namely, a neuropathic 
and an angiospastic diathesis, as being important in intermittent claudica¬ 
tion, he seems to have overlooked the possibilities above mentioned. Higier, 
himself, to whom he oft refers, was not clear as to the pathology of most of his 
cases. Amongst the latter’s cases can be recognized exquisite examples of 
thrombo-angiitis obliterans in the chronic or in the acute relapsing, stage. 
Just how important are the other predisposing moments to which Oppenheim 
alludes, to wit, the congenital Anlage or congenital mediocrity or inferiority 
of the vascular and nervous systems, it is impossible to say. 

In short, this author recognizes a “genuine” or true organic form of inter¬ 
mittent claudication and an angioneurotic. But even for the former variety 
he would postulate the existence of a congenital mediocrity or inferiority of 
the vascular system, a degenerative stigma that runs parallel with the neuro¬ 
pathic diathesis of these individuals. The finding of abnormally small 
femoral arteries in vivo during their exposure for the performance of the 
Wieting operation of arteriovenous anastomosis, convinced him of the cor¬ 
rectness of his hypothesis. 

III. Intermittent Claudication In Other Territories 

In fact a number of authors have observed phenomena attributable to 
occlusive conditions in the arteries of the affected parts, and Ortner 1 described 
what he calls: 

(a) Dyspragia Intermittens Angiosclerotica Intestinalis. 

In a male 55 years of age, an inveterate smoker, there were attacks of pain in the umbilical 
region 2 to 3 hours after a large meal, the symptoms lasting 2 to 3 hours. For several 
months there would be periods of intermission with recurrences. Exitus occurred after 
an operation. 

Autopsy showed marked atheroma of the aorta, the superior and inferior mesenteric 
arteries being markedly sclerotic. There was nothing else to account for the symptoms. 

Determann described a case of intermittent claudication, involving an arm, one lower 
extremity and the tongue. This latter case, however is open to the criticism that there 
were not multiple arterial obturations, but that some of the cerebral arteries were involved. 

(b) Intermittent Claudication of the Spinal Column. —Even an affection 
of the vessels of the spinal cord has been described by Dejerine, 2 who men- 

1 Ortner, Wien. klin. Wchnschr., 1902, p. 44. 

Ibid., Volkmann’s Vortrage, N. F., 347, Leipzig, 1903. 

2 Dejerine, Rev. neurol., 1906, 14, p. 341. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 

tions in the clinical picture an onset with cramp-like contracting sensations 
of heat and cold in one or both legs brought on by walking and disappearing 
after repose. With this, gradual aggravation of the symptoms, weakness 
after the slightest exertion become so accentuated that the legs are practi¬ 
cally functionally useless. Paralysis and evidences of contracture are absent. 
Increased reflexes and ankle clonus appear during the attack, as well as the 
Babinski reflex. Urinary and sexual disturbances may be associated, 
although sensory phenomena are absent. 

The histories reported by Dejerine 1 describe cases in the third or fourth 
decades with lower extremities that show no disturbances when in repose. 
After a short walk the limbs become heavy, motion more and more impaired 
until locomotion becomes impossible. Motor power returns after a few 
minutes of rest. Parasthesia, cramp-like sensation, formication, coldness 
and heat may be associated and also disappear during the period of rest. 

At the onset of this disease the patient must pause but rarely, being able 
to walk considerable distances, possibly even a mile, but later on the patient 
may require a rest after twenty or thirty steps. 

An ankle clonus, occasionally also a Babinski sign, that are absent, 
during rest can be elicited after motion. Occasionally urinary frequency and 
urgency and sexual hyperexcitability are associated symptoms. 

At the same time one can demonstrate all evidences of pathological altera¬ 
tions in the vessels; the pulses are present and also the vasomotor manifes¬ 
tations that usually accompany intermittent claudication. 

The prognosis is bad in these cases since a spastic paraplegia eventually 
develops. This outcome speaks for the assumption that an organic altera¬ 
tion is responsible for this affection. 

Dejerine believes that there is a deficient circulation in the dorsal portion 
of the lumbar cord by reason of a chronic arteritis. In all probability the 
permanent changes in the cord do not develop until a long period has elapsed 
since the history of the cases is long with marked remission in the 
symptomatology. 

Other authors, such as Grasset 2 and Sollier 3 have confirmed the above 
observations. In contradistinction to the two forms of dysbasia and angio- 
sclerotica intermittens, syphilis probably plays the most important part in 
determining endarterial lesions in the cord. 

Other authors, amongst whom Hardy, 4 Long, 5 and Rekord, 6 may be 
mentioned, have made similar observations. 

(c) Intermittent Claudication of the Upper Extremities. —The upper 
extremities may be the seat of similar phenomena. 7 The author has 
described their occurrence in thrombo-angiitis obliterans as well as in arterio¬ 
sclerotic lesions of the vessels. 

A number of cases have been reported in which the complex, intermittent 
claudication, involves both upper and lower extremities, with absent pulses in 
both. Whilst in some of these the findings would point to atherosclerotic 
vessels, in others the data given are not conclusive. 



1 Dejerine, These Paris, 1894, p. 179. 

2 Grasset, S., Rev. neurol., 1906, XIV, No. 10, p. 433. 

3 Sollier, Presse med., Oct., 1906, No. 85, p. 677. 

4 Hardy, Th£se de Paris, 1909. 

5 Long, Rev. med. de la Suisse romande, 1910, p. 7. 

6 Rekord, Amer. Jour. Med. Sc., 1912, 114, p. 721. 

7 Buerger, Loc. cit. 


148 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In the case of a man 58 years of age (Tobias 1 ) symptoms were present in both lower 
extremities and in the left arm. In the legs, there was a feeling of coldness and pain in the 
calf muscles upon walking, and for 1 year similar manifestations in the left arm. Striking 
was the early fatigue occasioned in the latter after using it. The intense feeling of coldness 
of the left hand necessitated the wearing of heavy gloves. . 

Physical examination showed an absence of the dorsalis pedis and posterior tibial pulses 
of both lower extremities; in the left upper, the axillary and subclavian pulsated, whilst 
all other large pulses were absent. 

Determann employs the term dyskinesia intermittens angiosclerotica to 
which the adjectives cruris and brachii are added for the leg and arms 
respectively. 

In a case of Nothnagel (1867) there was a thrombotic occlusion of the right 
axillary artery. 

In an arteriosclerotic woman of 25 the right axillary artery had been converted into a 
hard cord, easily palpable in the axilla and below this. The pulsation in the radial artery 
was absent, and in the ulnar and brachial there was but a slight beat. When the girl used 
the right arm even for the lightest kind of work, weakness soon resulted, with pain and 
paresthesiae in the hands and fingers. Work became impossible; after rest it could be begun 
again. It was not clear as to how the thrombus had developed in the artery. A somewhat 
insufficient collateral circulation had resulted. 

Whilst in the above-mentioned case extensive vascular disease was not 
present, but a localized thrombotic process was held responsible for the 
impaired circulation, other instances are reported where one or both upper 
extremities were involved in a manner similar to that of the lower extremities. 

In a case of Wedensky 2 the right arm was involved as follows: 

A male 38 years of age was suffering from intermittent claudication of the right leg, with 
symptoms also in the right arm. He could not write for any length of time without 
experiencing pain in the fingers and also in the wrist. At the same time there was hyper- 
hidrosis and later coldness of the whole right arm. In moderately cold weather the wrist 
and fingers would get blue. There were periods of improvement and intensification of the 
symptoms, until finally ulcers appeared on the second and third fingers, which, however, 
healed under treatment. At about this time gangrene of the third toe of the right foot 
occurred, necessitating exarticulation of the toe. 

Examination revealed the fact that the right arm was somewhat atrophic and colder 
than the left, and that the pulses in the right radial and ulnar arteries were absent. 

As a rule the symptoms in the upper extremities are associated with 
similar symptoms in the lower. Up to the year 1907, Bing was able to find 
about one dozen cases described in the literature. 

An interesting case is reported by Determann 3 where the tongue also gave 
symptoms. 

A Russian (Hebrew) who smoked 6 cigarettes a day complained, in addition to the 
usual symptoms in a leg and arm, of the following, very annoying manifestations: after 
speaking from 5 to 8 minutes, the mechanical act of articulation was impaired, although no 
interference with the mental functional mechanism was present. Gradually the tongue 
would become heavy and thick, motility returning after a short period of rest. The examina¬ 
tion of the lingual pulse revealed bilateral weakness. 

IV “Acute ” 4 Forms of Intermittent Claudication 

An inchoate, unreliable and unsatisfactory classification has resulted 
from the trend of a number of excellent observers to accentuate the impor¬ 
tance of the symptomatic association called intermittent claudication, and 

1 Tobias, Ztschr. f. d. ges. Neurol, u. Psychiat., 1921, 71, 309. 

2 Wedensky, Langenhecks Arch. f. klin. Chir., 1898, LVII, p. 98. 

3 Determann, Deutsch. Ztschr. f. Nervenh., 1905, XXIX, p. 152. 

4 “Acute” in quotation marks since this is an appellation of other authors. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 149 


also from a neglect of the pathologic basis or true morbid process. Some 
time prior 1 to such reports as to those of Higier 2 the author had already 
studied vascular material from identical cases, and had been able to recognize 
a clinical and pathological entity, to which the designation thrombo-angiitis 
obliterans had been given. Intermittent claudication was regarded as one of 
the manifestations of occluded arteries accompanying this as well as other 
maladies. 

The acute form of intermittent claudication of other authors corresponds 
to two essential vascular lesions; first, to the acute stage of thrombo-angiitis 
obliterans with sudden extension of the inflammatory and thrombotic 
obturation over varying territories; and second, to the deposition of keystone, 
parietal or even completely obliterating thrombosis in arteriosclerotic vessels. 

(a) Acute Stage of Thrombo-angiitis Obliterans. —The contributions to 
the literature of “ acute intermittent claudication ” have added considerably to 
the clinical confusion already sufficiently ingrained and impressed by multitu¬ 
dinous and variant descriptions of types of intermittent claudication. Whilst 
Higier 3 reports a clinical picture of subacute or chronic course as intermittent 
claudication or angiosclerotic paroxysmal myasthenia in one publication, 
he speaks of “arteritis acuta with intermittent claudication” elsewhere, 4 
when the onset of the malady is sudden. In the former 5 he was, we believe, 
dealing for the most part with cases of thrombo-angiitis obliterans of the 
chronic progressive type; in the latter, with the same malady during a period 
of acute manifestations. In neither instance, was this author justified in 
speaking of a disease “intermittent claudication.” 

The case of Higier 6 reported in 1910 corresponds with the author’s “acute 
stage” or acute thrombotic exacerbation in thrombo-angiitis, and can in no 
sense be regarded as a rarity. He cites the following history. 

A Polish Hebrew, 25 years of age was suddenly seized with pain in the right foot. 
Fever, chills and general depression were absent at the onset, and there was no local swelling, 
abnormal redness or heat, abnormal pallor, cyanosis or coldness. Examination of the 
internal organs was negative. There was no increased blood pressure and no anemia. 
The urine was free of albumin and sugar. Intense pain in the right foot and leg made 
walking impossible, but abated with the patient in bed and at rest. Walking, even after 
some 30 or 40 paces, produced a feeling of numbness and fatigue in the calf of the leg, 
necessitating immediate cessation of locomotion. A certain degree of pallor of the foot 
seemed to follow repeated or prolonged movements of the extremity, whereas the pendent 
foot turned to a livid or rose color (erythromelia). The temperature of the extremity was 
lowered. The right dorsalis pedis and posterior tibial arteries did not pulsate. Later, 
exceedingly painful ulcers of the second and third toes developed. Radiography showed 
no arterial calcification. The pulses of the leg were present. In the past history nothing 
of moment could be elicited, no lues, no exposure to cold nor to trauma. 

The insomnia which did not respond to sedatives and hypnotics made the patient desper¬ 
ate and he was anxious to accept the physician’s proposal of amputation. However, after 
three months the ulcers healed, and the pain as well as the intermittent claudication 
diminished greatly. Six weeks later he was able to get up. 

The physical examination made about ten months after the first symptoms, showed 
persisting coldness, moderate lividity of the foot, and absence of the pulses. 

In the light of the author’s 7 studies, and in a comparison with almost 
identical observations in which pathological material through amputation 

1 Buerger, Amer. Jour. Med. Sc., Oct., 1908; Proc. New York Path. Soc., March, 1908. 

2 Neurol. Centralbl., 1910, p. 911. 

3 Higier, Deutsch. Ztschr. f. Nervenh., 1901, XIX, p. 439. 

4 Higier, Neurol. Zentralbl., 1910, XXIX, p. 911. 

1 See “Intermittent Claudication,” p. 255. 

6 Higier, Neurol. Centralbl., 1910, XXIX, p. 912. 

7 Buerger, see literature on Thrombo-angiitis obliterans. 


150 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


was available for study, there can hardly be any doubt but that the case 
reported by Higier was one of thrombo-angiitis olbiterans. That extensive 
acute inflammatory thromboses occur throughout the territory of the dorsalis 
pedis, posterior tibial, peroneal and popliteal arteries in thrombo-angiitis oblit¬ 
erans, the author has demonstrated beyond the shadow of a doubt. And, the 
manifestations called forth correspond in almost every detail to those in the 

story above related. , , 

How misleading an attempted grouping of unrelated diseases under the 
caption “Intermittent claudication” can be, is well illustrated both by 
Erb’s quest for a special category in which to put the so-called “ acute form of 
intermittent claudication,” and Higier’s renewed necessity for separation of 
his “angiosklerotische paroxysmale Myasthenie” from the “acute type 
subsequently called “arteritis acuta with intermittent claudication. 

(b) Arteriosclerosis with Thromboses Diagnosticated as Acute Intermit¬ 
tent Claudication. —Elsewhere will be described a characteristic picture of 
“acute attacks of thrombosis” in cases with arteriosclerotic vessels (Chap. 
LXIX). In some of these intermittent claudication has preceded by many 
months or years; in others, no clinical evidence of vascular affection has made 
itself manifest. When, therefore, a patient with no past history referable 
to the lower extremities, suddenly develops intermittent claudication or other 
phenomena resulting from vascular occlusion, a thrombotic lesion is the 
most probable cause , although palpatory evidences of such occurrence may be 
absent. Cases such as that reported by Pelnar 1 may be classified from the 
pathologic standpoint as latent arteriosclerotic vascular lesions with second¬ 
ary parietal and occlusive thromboses. The history report may be 
summarized thus:— 


An engineer, 61 years of age, developed the following symptoms rather rapidly. After 
walking but a few (2 to 3) steps he experienced a peculiar uncomfortable sensation in the 
whole left lower extremity, as if the limb were foreign to him, this feeling gradually giving 
way to heaviness and lack of control of the affected part. This necessitated pausing to 
rest, immediate recurrence of these manifestations following renewed attempts to move 
about. So severely was he affected that only the most necessary steps were taken, the 
sitting posture offering considerable relief. 

His wife noted that his toes would be cold, pale and “like dead, the left leg colder than 
the right. Because of tenderness in the left groin, the respective region was protected from 
all pressure and contact. There had been a previous history of mild apoplectiform attack 
with recovery. . 

Physical examination November 5, 1909, revealed increased blood pressure (180 mm. 
systolic) generalized arteriosclerosis, and cardiac enlargement. The femoral artery 
below Poupart’s ligament was tender and its pulsation weaker than that of the other side. 
The left dorsalis pedis beat was also diminished. 

Iodides were administered and in 1 month the subjective symptoms abated consider¬ 
ably, and walking became easier. So also the tenderness in the groin became limited to a 
small area. Objective signs remained stationary and the blood pressure rose to 210 mm. 
(systolic). _ . , , , 

In August, 1910, he was again seen and found to be suffering from the results of an 
apoplexy whose onset was recorded as January, 1910. The right side was the seat of slight 
paresis. The symptoms in the left lower extremity were noticeable only after prolonged 
exertion and locomotion, and were of only moderate degree. The left femoral and popliteal 
beats were weak, whilst the dorsalis pedis artery could “hardly be felt.” 


In short, a case of marked arteriosclerosis, high blood pressure, apoplecti¬ 
form attacks, with rather sudden advent of enfeebled pulsations, the arterial 
distribution of the left lower extremity being accompanied by the usual symp¬ 
toms of intermittent claudication with gradual improvement and practical 
disappearance of the dorsalis pedis pulse. Such examples have frequently 


1 Pelnar, Neurol. Zentralbl., 1911, XXX, p. 9. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 151 


been observed by the author, and when gangrene eventuates—as occurs in a 
certain percentage of the cases—the existence of thrombosis superimposed 
upon the arteriosclerotic lesion has been demonstrable at autopsy or dissec¬ 
tion of the amputated limb. 

Doubtless parietal, keystone, and completely occlusive thrombi are re¬ 
sponsible for similar clinical pictures. Syphilis also, and still unknown forms 
of arteritis —(thrombo-angiitis obliterans being a distinctive, well differenti¬ 
ated type), by virtue of complicating thrombosis and obstructive impairment 
of the circulation can give rise to like symptom-complexes. 

V. Apokamnosis (Goldflam 1 ) or Artificial Intermittent Claudication 

Goldflam employed this term to denote abnormal liability to fatigue in 
myasthenia, and transferred its application so as to designate also a feeling 
of tiredness, numbness, heaviness and tension evoked by actively lifting the 
affected limb. Whilst these manifestations can be artificially induced in an 
extremity in which intermittent claudication occurs, in the normal only 
slight pain or a feeling of fatigue will be tardily produced. Latent cases of 
intermittent claudication may be brought to light by this test—instances in 
which the typical signs have not as yet developed—and in which pallor, 
rubor and cyanosis may dominate the clinical picture. As a comparative 
method of investigating two corresponding limbs, it may reveal sufficient 
differences to be of diagnostic worth. 

Artificial pallor is also producible in cases with symptoms of intermittent 
claudication, if the foot—whilst in the horizontal position—be flexed and 
extended some thirty to forty times. The color contrast is even more strik¬ 
ingly forthcoming, if the leg be permitted to hang down when the exercises 
are carried out. Blanching of the fingers and hand can also be made to 
occur by repeated flexion and extension of the fingers with arms hanging. 
But most noteworthy is the ischemia of the foot following walking, particu¬ 
larly if a test of locomotion be tried after the patient has been standing for 
some time. 

Goldflam attempts to explain the cutaneous ischemia in the following 
manner. With the active motion of the extremity and the implied muscular 
contractions, a hyperemia of this territory with dilatation of the arteries 
occurs. With this “functional hyperemia” of the muscular vessels, a 
collateral cutaneous anemia is to be expected. Invoking also the participa¬ 
tion of the vasomotor nervous system, he calls attention to the autonomous 
self-regulating mechanism that is an inherent role of its activities, so that 
with the necessary dilatation of the deep arteries a corresponding constric¬ 
tion of the capillaries and arterioles of the integument, is an essential compen¬ 
satory sequence. 


PATHOLOGY 

A study of the literature is exceedingly unsatisfactory, because of the 
fact that authors have not differentiated between the obliterating lesions of 
arteriosclerosis those of so called “endarteritis obliterans,” and the 
obturating process of thrombo-angiitis obliterans. The failure to properly 
interpret the histological picture resulting from the canalization and vasculari¬ 
zation of obturating thrombi has produced confusion in the literature; no 
cognizance having been taken of that special, inflammatory and thrombotic 
1 Goldflam, Neurol. Zentralbl., 1910, XXIX, p. 2. 


152 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

lesion described by the author. In fact, the lack of distinguishing criteria 
between arteriosclerosis, endarteritis obliterans and thrombo-angiitis 
obliterans, has permitted an incorrect conception of the pathology of these 
conditions to persist. 

Thus, the cases of Charcot, Dutil and Lamy, 1 Laveran, 2 Panas, 3 Goldfiam 
Erb, and others are described by authors who have made a critical study of 
their publications, as examples of a productive or obliterating endarteritis. 
Endarteritis obliterans in this sense is considered to be a progressive thicken¬ 
ing of the intima, through proliferation of a cellular, new-formed connective 
tissue, leading to complete closure of the arterial lumen. 

This interpretation is incorrect, for, some of the cases mentioned are 
examples of arteriosclerosis, others of syphilitic endarteritis, and still others 
of thrombo-angiitis obliterans. 

Bing 4 in his resume of intermittent claudication is unable to differentiate 
between endarteritis obliterans of Friedlander—which in all probability is 
identical with thrombo-angiitis obliterans—and that of arteriosclerosis. 
Be that as it may, it can be gleaned from the literature, that in spite of 
uncertainty as to the exact pathological nature of the obstructive arterial 
conditions observed, most authors are in accord in the opinion that organic 
impoverishment of the circulation by an obturating vascular affection is 
usually the pathological substratum. 

In the consideration and treatment of the subject of etiology and 
pathogenesis, the lack of proper recognition and segregation of types of 
pathological process have also entered into the production of inexplicable and 
conflicting statements and circumstances on the parts of various authors. It 
can therefore be readily understood how the views of one observer who de¬ 
scribed only the arteriosclerotic form of intermittent claudication can be 
diametrically opposed to those of another author dealing with cases of thrombo¬ 
angiitis obliterans, as to the question of the particular age at which the 
process is most apt to occur. In the former, older individuals, in the latter 
the young, and predominatingly the Hebrew race will be affected. It is 
just this inability to differentiate between the types of cases that has called 
forth much academic discussion and many controversial argumentative 
publications. 

Causal agents of varied nature such as chemical toxins, static, and even 
neurotic influences have received the attention and recognition of 
commentators on this subject. 

According to one set of statistics regarding age (Erb), there were but 3 
cases under 30 years; from 30 to 40, there were 9; from 40 to 50 years, 20; 
from 50 to 60 years, 27; and from 60 to 70 years, 14 patients. So the largest 
number occurred between 40 to 60, the age at which arteriosclerosis is most 
pronounced. 

Some authors report cases in even young individuals. Higier 5 and 
Idelsohn 6 cite such cases in young people, the latter also referring to a patient 
34 years of age. Some of these were doubtlessly cases of thrombo-angiitis 
obliterans. Indeed, Higier concludes that of his 23 cases at least one-half 
were under the age of 40. 

1 Dutil and Lamy, Arch, de med. exper. d’anat. path., 1893, p. 102. 

2 Laveran, Acad, de Med. Seance du 27 fev., 1894. 

3 Panas, Acad, de Med. Seance du 5 juin, 1894. Sem. med., 1894, p. 265. 

4 Bing, Beiheft z. med. Klin., 1907, p. 117. 

5 Higier, Loc. cit. 

6 Idelsohn, Deutsch. Ztschr. f. Nervenh., 23, S. 285. 


DIAGNOSTIC SYMPTOMS— INTERMITTENT CLAUDICATION 153 


The affection occurs more frequently in men than in women, and accord¬ 
ing to Erb there were but 9 cases in females amongst his 168 cases. The 
Hebrew race is said to be particularly predisposed, as well as the inhabitants 
of East Russia, Poland, the Baltic Provinces and Finland. 

Excessive use of tobacco is cited by Erb as one of the most important 
causal factors, and he gives the following statistics: 

Of 500 males taken from the better classes, who did not present the symp¬ 
toms of intermittent claudication, 4 classes could be distinguished according 
to indulgence in tobacco (smoking), as follows: 

Non-smokers or almost non-smokers; a second class of moderate smokers (3 to 6 cigars or 
10 to 15 cigarettes); a third class (7 to 12 cigars or 15 to 40 cigarettes); and the fourth class 
of excessive smokers (40 to 100 cigarettes). Of the 500 males, 44.8 belong to the first class, 
31.6 to the second, 17.8 to the third, and 5.8 to the fourth. Of the cases of intermittent 
claudication, however, 7 per cent belong to the first class, 14 per cent to the second, 50 per 
cent to the third, and 28.6 per cent to the fourth. From these statistics one may conclude 
that there is a preponderance of smokers amongst patients suffering from intermittent 
claudication. 

Idelsohn attached some importance to the existence of flat feet in certain cases. Deter- 
mann observed a hereditary tendency to arteriosclerosis in one family, and a neuropathic or 
neuro-angiospastic disposition is held by others to play a significant role. 

A neuropathic habitus is regarded by Oppenheim, Erb and Goldflam, as 
of some importance as a contributing etiologic factor. Its frequent incidence 
in Hebrews and the coexistence of hereditary psychoses, congenital anomalies 
and functional neuroses have given weight to this view. Oppenheim has 
suggested that an angiospastic disposition is not uncommonly associated with 
intermittent claudication, and further inclined to the hypothesis that a con¬ 
genital narrowness of the arterial system may be in some way related to such 
vasomotor inclination. 

In another publication Erb concludes that intermittent claudication corresponds in the 
age at which it afflicts individuals with the period during which arteriosclerosis is most 
apt to occur. A preponderating number of his cases was over 40 years of age. Of 57 
cases only 1 was under 30 years; between 30 and 40 there were 8; between 40 and 50 there 
were 19; between 50 and 60 there were 20; and over 60 years there were 9 cases. 

Higier (whose views have been considered elsewhere) and who undoubtedly had for the 
most part cases of thrombo-angiitis obliterans under observation, reported that of 23 cases, 
50 per cent were under 40 years of age. 

The mere fact that the intermittent claudication described by all of these 
authors is extended to include the totality of symptoms in a number of different 
pathological processes, and in the case of Erb said to be connected with 
arteriosclerosis of the vessels of the lower extremities, and in the case of 
Higier to correspond to the disease, thrombo-angiitis obliterans—is sufficient 
argument in favor of the view oft expressed by the author, that associated 
symptoms common to a number of different lesions and morbid processes 
must not be exalted into the equivalent of the morbid processes themselves. 

Had some of these observers the opportunity of being convinced of the 
absolute pathologic differences that underlie the vascular obturation in the 
various cases, their classification would in all probability have been carried 
out on a pathologic rather than on a clinical foundation. 

The circumstance that the symptoms of intermittent claudication may be 
absent in cases of outspoken arterial disease, suggests the importance of a 
functional factor—an angiospastic condition—as responsible for the symp¬ 
toms. So Erb concludes that the necessary vasodilatation that normally is a 
concomitant of increased function is absent in these cases, and even accepts 
the possibility of vasoconstriction in the pathologically changed vessels. So 


154 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

also is Bing willing to agree in this assumption basing his view upon the 
significance of the ischemia and cyanosis of the skin—phenomena dependent 

upon vasomotor action. . , . 

We shall discuss these matters critically in another section, and it may 
suffice here to say that whilst these views may be correct in part, they lack 
foundation insofar as vasoconstriction of the obliterated vessels is incon¬ 
ceivable. However, that an additional moment, namely, a vasomotor 
process is active in other vessels, that is, in the normally patent vessels, be 
they of the skin or of the subcutaneous tissues, or unmvolved muscular 
vessels, is not only possible, but undoubtedly takes place. It occurs m two 

types of cases. . . . .. . 

Firstly, in cases in which the symptoms of intermittent claudication are 
dependent upon and associated with marked obliteration of some or many of 

the large vessels and . . 

Secondly, cases in which the patency of the larger vessels is unimpaired. 


CRITICAL SUMMARY 

When described as a clinical entity by certain authors (Higier, Idelsohn, 
Kahn, Kohler), the symptomatology will be found to correspond to patho¬ 
logic processes of different nature and to be inclusive not only of thrombo¬ 
angiitis obliterans, arteriosclerosis of the vessels of the extremities, but also of 
certain vasomotor affections of doubtful nature. Let us summarize the 
symptomatic history as described by these and other authors, so as to illus¬ 
trate most vividly the misconceptions that such a grouping will create. 
Then only will the fallaciousness and incoherency of a mere clinical associa¬ 
tion of wholly unrelated morbid processes, be well appreciated. 

Thus Cassirer 1 summarizes the course of intermittent claudication as follows: 
“The malady (intermittent claudication) usually takes a chronic course, 
although the severe symptoms may arise rather suddenly. Prodromal 
signs are usually to be observed. The symptoms, the paresthesiae, pain, 
tension, gradually increase to the severity of well marked intermittent 
claudication that materially intereferes with occupation.” 

In this very first descriptive paragraph, the simultaneous usage of the 
appellation, intermittent claudication, both as a noun and as an attribute or 
adjective, is illuminating. Then follows: “If now, an arrest cannot be 
brought about through correct therapy and diet, progressive gangrene of the 
toes, of the foot or of the leg with the usual severe consequences, is the issue. 
Sometimes a stationary period intervenes after gradual improvement; an 
adequate collateral circulation may be developed or the arteriosclerosis may 
abate ^ 

Such a clinical picture is no more applicable to intermittent claudication 
than it is to any of the other striking phenomena of obstructive vascular 
disease of the extremities. It corresponds to arteriosclerosis, as well as to 
thrombo-angiitis obliterans and other types of thrombotic lesion. By the 
same token, and by similar reasoning, ruhor or erythromelia, or ischemia , 
mere manifestations, may be elevated and exalted into the rank of separate 
maladies. For both of these examples, mentioned to illustrate by analogy, 
are just as frequent concomitants of obstructive arterial processes as is 
“intermittent claudication.” 


1 Cassirer, Loc. cit. 


DIAGNOSTIC SYMPTOMS—INTERMITTENT CLAUDICATION 155 


The pathognomonic evidence of intermittent claudication is termed 
“paroxysmal myasthenia” by Higier . 1 He describes the typical phenomena 
just as Erb and Cassirer have, and adds that for diagnostic purposes, the 
coincidence of weakness or absence of pulses in the affected territories is an 
essential accompaniment of the paroxysmal recurrent dysbasia. He, too, 
therefore, accepts an anatomical pathological substratum in the arteries 
as the basic lesion. 

Indeed, a study of Higier’s article 2 on “ Angiosclerotic Paroxysmal Myas¬ 
thenia (claudication intermittente of Charcot) and Spontaneous Gangrene” 
will engender the conviction in any observer conversant with the disease 
thrombo-angiitis obliterans, that the latter malady and not intermittent 
claudication had come under that author’s observation. Although he recog¬ 
nized the existence of a vascular affection in his cases, a lack of pathological 
material is responsible for his view that a neuropathic diathesis plays the most 
important role in the symptomatology. Conceding to functional neurotic 
factors a preponderating influence in the clinical manifestations, he neverthe¬ 
less recognizes the existence of arterial disease and secondary nerve degenera¬ 
tion. That his own conception of the interrelationship between arterial 
affection and intermittent claudication is discordant and at variance with the 
author’s is to be gleaned from his belief that the vascular processes are 
secondary in some cases to a primary nerve lesion . 


EXPLANATION OF PHENOMENA 

Many explanations have been given to account for the symptoms induced 
by exercise, most authors invoking a vascular spasm as the most plausible. 

Such vasoconstriction would be pathological, since our physiological 
concepts presuppose dilatation as a response to excessive demands. Some 
assume that an abnormal vasoconstriction or reflex is the reaction of patho¬ 
logical arteries. This view is, however, not altogether satisfactory, firstly 
because the diseased vessels in blocked territories (such as thrombo-angiitis 
obliterans) must surely have lost their contractile powers, and secondly, 
since the more peripheral disturbances in the supplied muscles and other 
tissues are then not taken into account as a possible source of origin for special 
or abnormal reflexes. 

Intermittent Claudication with Healthy Arteries.—Zak has shown 3 that * 
identical symptoms are producible after exercise in a normal upper extremity 
when the brachial artery is artifically compressed. 

If the brachial artery be compressed with the finger with the arm in a horizontal 
position, and then repeated opening and closing of the hand be carried out some 30 or more 
times, increasing weakness and fatigue set in; on further motion a cramp-like sensation 
appears in the hand up to the wrist, and later such pain as to make flexion and extension 
impossible. Simultaneously a cadaveric hue of all five fingers develops, which is limited 
about at the metacarpal phalangeal level, or extends somewhat up the dorsum of the hand. 
Sometimes the pain extends up to the elbow, together with a sensation of fatigue. 

When the blood is allowed to enter again, a typical red hyperemia (reactionary) takes 
place over the arm and hand, but the pallor of the fingers may persist for 10 or more 
seconds, yielding gradually to pale pinkish or rose colored patches. 

This experimentally or artificially induced symptom-complex is compar¬ 
able to that of intermittent claudication, and can be demonstrated to occur 

1 Higier, H., Zur klinik d. angiosklerotische paroxysmalen Myasthenia, etc., Deutsche 
Zeitschr. f. Nervenheilk, 1901, 19, pp. 438-466. 

2 Loc. Idem. 

3 Zak, Wien. Arch. f. inn. Med., 1921, 2, p. 408. 


156 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


with vessels altogether healthy. Explanations for the genesis of the phenom¬ 
ena, other than reflexes emanating from the diseased vessels themselves, 

therefore must be resorted to. . . . 

Not only can the sensory manifestations of intermittent claudication 
be stimulated in the above way, but data seem to indicate that in an ischemic 
limb, conditions are at hand which predispose to angiospasm or heightened 
vasoconstriction of the small vessels as the result of exertion. 


And so it has been observed that whereas the resting limb will react (reactionary hyper¬ 
emia) in a sudden fashion upon the release of an Esmarch bandage or compression of a main 
nutrient artery, a considerable delay of this vasodilating response, and a persistence of 
vasoconstriction occur, if such an artificially ischemic limb be allowed to exercise. From 
this it has been concluded that a state of vasoconstriction or spasm in a multitude ot vessels 
in the ischemic vascular territory, responding in this heightened way to exercise, may be 
responsible for the symptom-complex, intermittent claudication. 


Theories as to the Cause of the Angiospasm.—More recent views tend to 
the acceptance of a chemical or chemiconeuro reflex explanation. When the 
main artery of a limb is compressed or an Esmarch bandage or a tourniquet 
is applied, a consequent ischemia or anemia depends not only upon a lack of 
blood in the arterioles and capillaries, but also upon arterial constriction. 
This is demonstrated by the author as obtaining in thrombo-angiitis obliterans 
upon elevation of the affected extremity. The small vessels do not collapse 
in their true sense, but contract—possibly a functional response or defense 
against reflux or venous blood. Indeed, Hering concludes that venous blood 
exercises a vasoconstricting influence on the arterial wall. 


The R 61 e of Chemicals in an Anemic Territory.—Many other data 1 discovered by 
physiologists have disclosed the influence of chemicals on the contractility of the smaller 
blood vessels. Fleisch 2 showed that weak concentration of carbon dioxid causes vascular 
dilatation, whilst strong concentration causes contraction. Dearth of oxygen causes 
vasoconstriction. Thus, it has been assumed that the diminution of oxygen may be 
responsible for vascular constriction. Not only a direct chemical effect upon the arteries 
has been thus revealed, but even an indirect vessel reflex through nervous influences was 
demonstrated by the author; for similar contraction was produced in territories only in 
nerve connection with that in which carbon dioxid accumulation has been experimentally 
produced. 

Therefore, two antagonistic reflexes may be at play in a member, whose 
circulation has been put in abeyance but allowed to exercise; firstly, the 
normal vascular dilating reflex of a functionating part with normal circulation; 
and secondly, a vasoconstricting one, which is especially active in the badly 
nourished territory. In the latter accumulation of carbon dioxid or defi¬ 
ciency in oxygen may account for the abnormal reflex. When the constricting 
influence overbalances the dilating, the subjective and objective phenomena 
of intermittent claudication may be produced. In the presence of increased 
carbon dioxid concentration and deficiency in oxygen, a normal vaso¬ 
dilating response is diminished or put in abeyance. This is the theory 
advanced by some of the more recent observers. 

More recent work (Hopkins 3 ) emphasizes the importance of the develop¬ 
ment of lactic acid in muscle physiology. The prime, if not the sole, cause 
of fatigue in muscle is believed to be the accumulation of this acid. Although 
the author has been unable to find any investigations of illuminating nature 
regarding the direct effects of lactic acid in evoking a vasoconstrictor reflex 
action, the general trend of interpretations seems to regard the deficiency of 


1 See Capillary Circulation. 

2 Fleisch, Pfliigers Arch., 1918, Bd. 171. 

3 Hopkins, Harvey Lectures, April 2, 1921 (Lippincott). 


FORMS OF GANGRENE 


157 


oxygen and the accumulation of acid waste products as responsible; lactic acid 
would be one of these. 

Whether failure to eliminate lactic acid and the consequent change in the 
elastic properties of the muscles may be translated into a direct response in 
sensory nerves , without implication of vasomotor mechanism, is another 
hypothesis worthy of consideration. It would presuppose a direct analogy 
between the cramp-like pain of excessive fatigue in healthy, well nourished 
tissues, and the symptoms of intermittent claudication, both explicable in the 
light of the above theory. 

DIFFERENTIAL DIAGNOSIS 

1. Myasthenia Gravis Pseudo paralytica .—In this affection, too, we also 
note an intermittent disturbance of motor function that returns with each and 
every exertion, but is distributed over wide muscle territory, is characterized 
by a typical electrical reaction, and is unaccompanied by sensory or vasomotor 
phenomena. 

2. Dysbasia Neurasthenica .—This type is somewhat more difficult to 
diagnosticate particularly from intermittent claudication of the spinal cord. 

Charcot cites an example of a lieutenant who could walk fairly well in the normal 
march, but at a faster pace would become unsteady after 20 to 30 minutes, his right limb 
particularly becoming heavy. With this there was marked numbness of the sole of the foot; 
all of the symptoms disappeared after rest. The patient, who was markedly neuropathic, 
was neither arteriosclerotic, leu tic, nor diabetic. Objectively the pulses were negative and 
vasomotor phenomena absent. The knee reflexes were increased, and there was a right 
sided ankle clonus. Because of the marked neurasthenia, an affection of the spinal cord 
was believed to be absent. This diagnosis was confirmed 7 years later by Bourgeois, who 
observed that the same patient was still unable to carry on his activities. 

3. Sciatica .—Here we must consider those relatively mild cases of sciatica 
in which paroxysmal attacks of pain are evoked only by motion, and call forth 
restriction of function. The pain in these patients does not abate as quickly 
as in intermittent claudication, and furthermore during the free intervals, 
pressure on Walleix’s point should provoke the latent pain. 

4. Akinesia Alger a .—In this psychasthenic affection pain is aroused 
immediately upon the beginning of motion, and can occur not only in the 
extremities, but also in the back, in the head and elsewhere. 

5. Tarsalgia and Metatarsalgia .—Here too pain follows short periods of 
locomotion and is localized to the tarsus and metatarsus. The arteries are 
intact and vasomotor phenomena are absent. There is usually a circum¬ 
scribed area of tenderness. 

6. Certain Rare Cases of Neuritis .—Cases have been described by Hallion 
and Charcot 1 as examples of neuritis, but the histories are not convincing, 
since the evidences of arterial involvement are sufficient to make it impossible 
to exclude these as a factor in the symptomatology. 


CHAPTER XXVII 

FORMS OF GANGRENE 

One of the oldest classifications and one which has but little value since 
it throws no light upon the etiology, is the subdivision into dry and moist 
gangrene. Some authors add another variety, microbic gangrene. 

1 Hallion and J. B. Charcot, Arch, de Neurol., Feb. 28, 1895, XXIX, p. 81. 



158 CIRCULATORY AFFECTIONS OF TIIE EXTREMITIES 

Dry gangrene ensues when the arterial circulation is suddenly impeded 
while the venous flow continues, the tissues being drained of their fluid 
through the veins. Mummification follows and the part becomes desiccated 
or dry by reason of loss of water. In man it is usually the peripheral parts 
that are affected. Perhaps mummification is a more' descriptive word. 
This variety is not infrequently met with in the aged, when, by virtue of the 
slow process of athero- or arteriosclerosis, the lumina of the arteries become 
occluded, the blood supply diminishes progressively, and finally gangrene of a 
distal part occurs. Although the words senile and dry gangrene have at times 
been used synonymously, this restricted application of the term is incorrect, 
since dry gangrene takes place in many other conditions. 

After preliminary blanching, paresthesiae, coldness and loss of sensation, 
cyanosis usually follows. The skin gradually becomes dry, then brownish or 
black, the whole part being converted into a shriveled, hard, blackish mass. 
The changes in color are ascribed to the disintegration of hemoglobin with 
the elaboration of black by-products. 

Moist Gangrene .—Moist gangrene results when there is an impediment 
both to the influx of arterial blood and to the venous return, so that the 
affected part retains sufficient fluid to leave the dead tissues moist. Com- 
plete obstruction of the chief veins of a part, without occlusion of the 
arteries, may also lead to gangrene, although this is of rare occurrence. 
The condition of the circulation in the limb before the arrest of arterial cir¬ 
culation takes place, may be the determining factor in the production of 
either the moist or dry type of gangrene. Intense edema associated with 
nephritis or impaired heart action usually favors the development of moist 
gangrene, as in the embolic or thrombotic gangrene, complicating pneumonia 
or other infections. 

Because of the putrefactive condition characteristic of this process, 
putrid gangrene would be an apt designation. The sequence of events is first 
degeneration of the blood with the appearance of dirty red patches and 
zones. Then the connective tissue and muscles undergo change, whilst 
epithelium, tendons, elastic fibers, cartilage, and bone are most resistant. 

The parts become doughy, edematous, the epidermis is separated off in 
blebs; there may be gas formation (NH 3 , SH 2 , or S (NH4)2), crepitation and 
foul odor. Leucin, tyrosin, triple phosphates, blackish pigment and fat 
crystals are to be found in the fluids. In addition to putrefactive organisms, 
streptococci often develop and may enter the blood stream. Bacillus coli 
may also be associated, and the bacillus proteus vulgaris may grow in 
symbiosis with either of the above and enhance their virulence. 

The general clinical picture is an expression of the absorption of toxins 
(especially of proteus) with or without the effects of streptococcus or bacillus 
coli bacteriemia. 

Characteristic for moist gangrene are the following clinical stages: 
first, a stage of pallor which may pass so rapidly as to be overlooked; second, 
a stage of extensive ecchymosis; third, a stage of subepidermal exudation with 
reddish discoloration of the part; and fourth, a stage of disintegration. 

Although these stages are not always clearly defined, they may be recog¬ 
nized in a fairly large percentage of the cases. The initial pallor may be 
evanescent; it may be accompanied with paresthesiae but more regularly 
with frigidity and anesthesia. Soon a bluish and purplish mottling that 
rapidly spreads over the affected part becomes the striking objective mani¬ 
festation, being succeeded by the exudation of bloody serum under the epi¬ 
dermis. When the latter is lifted off, larger or smaller bullae are formed 


PLATE I 





Early Stage of Moist Gangrene, Showing Bullae. (Buerger in Ochsner’s ‘‘Surgery,” 

Vol. IV.) 





PLATE II 



Later Stage of Moist Gangrene. (Buerger in Ochsner’s “Surgery,” Yol. IV.) 








PLATE III 



Third Phase in the Appearance of Moist Gangrene. (Buerger in Ochsner’s “Surgery, 

1 r \ 7^1 1\ 7 \ 






































FORMS OF GANGRENE 


159 


(Plate I) many of which attain considerable size. When the epidermis has 
been separated and no considerable fluid is present, the angry red cutis vera 
shines through (Plate II). Higher up, the limb is usually cold for a variable 
distance, often intensely edematous and brawny, mottled here and there by 
areas of purplish discoloration (ecchymosis). Later the intense red dis¬ 
appears, as the disintegrating cutis vera and the gray green epidermis com¬ 
bine to form a peculiar ashen purplish hue (Plate III). The serum from the 
bullae now makes its escape in many places, the separated epidermis lying in 
folds over it, here and there torn off, exposing the weeping derma. With the 
advent of putrefaction, an intensely foul odor develops. Secondary pyogenic 
infection complicated by lymphangitis and cellulitis above the site of gang¬ 
rene may supervene and be associated with toxic general symptoms. 

Microbic gangrene has been termed acute microbic gangrene, fulminating 
gangrene, emphysematous gangrene and traumatic spreading gangrene. 
Here a virulent infection usually with a gas producing micro-organism is 
responsible for the mortifying process, injury usually preceding the infection. 

If descriptions of this type be taken from older authors, a rather confused 
clinical picture will be obtained. Latterly, our notions have been consider¬ 
ably clarified since advances have been made in bacteriologic recognition 
of varying types. Special attention has been focussed on the gas-bacillus 
forms of infection, which will be discussed at length in another chapter. A 
number of different micro-organisms have been isolated and identified as 
the causative agents in this severe form of infectious and gangrenous process. 

There is still another “ infectious ” or microbic type of gangrene in which 
gas formation is absent and in which the streptococcus can often be isolated 
in pure culture. A more comprehensive description of this variety will also 
be given elsewhere. 

Course and Termination. —Gangrene is very frequently self-limiting, a 
definite line, separating the dead and the living tissue known as the line of 
demarcation , being ultimately formed. At this line granulation tissue is 
developed, as the result of a reactive inflammatory process. By virtue of the 
action of the emigrated leukocytes, certain ferments are elaborated which 
bring about the separation of the dead from the healthy tissue. Soft parts 
yield relatively soon to the sequestrating effects of the inflammatory process, 
whilst bone is very much resistant. When a considerable part of a 
member is thus separated off, so-called spontaneous amputation results. 

When the area of necrosis or mortification is infected, the process of sepa¬ 
ration is accomplished in a different manner. The usual phenomena of sup¬ 
purative inflammation of greater or lesser virulence are manifest, the products 
of inflammation being instrumental in causing disintegration of the part at its 
junction with the living, but may also spread in the healthy tissues requiring 
surgical intervention. If sufficiently severe, a rapidly ascending lymphangi¬ 
tis may occur, general infection, bacteriemia and toxemia. In these cases the 
end-result will depend upon the virulence of infection, and of the possibility 
of its control. 


160 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XXVIII 

CLASSIFICATION OF GANGRENE 

From the clinical standpoint, a pathological and etiological grouping is most 
satisfactory. It must be remembered, however, that an absolute classifica¬ 
tion is impossible, both because case may simultaneously belong to several 
groups, and because the causative factor in certain instances is not well 
understood. 

Three large groups may be recognized: first, gangrene due to external or 
direct causes, such as bring about immediate death of tissue; second, gangrene 
due to internal or indirect causes, which act by impeding or arresting the 
circulation of blood in the larger vascular channels; and third, neuropathic 
gangrene in which the cause is an abnormal, pathological, functioning vaso¬ 
motor nervous mechanism, or resides in the vegetative nerves. 

A. External or Direct Causes.—(i) Mechanical Causes in which death or 
necrosis is the direct result of the physical injury. Tissues may become 
completely separated in continuity and thus die; or, necrose because of the 
disorganizing effect of a crushing force. Continuous pressure upon bony 
prominences, particularly in the emaciated, produces gangrene or necrosis 
to which the name decubitus has been given. Compression by a tight bandage, 
torsion acting upon a portion of the intestine, or strangulation at the neck of a 
hernial sac—all are mechanical causes of gangrene. 

2. Thermic Causes, intense heat or cold, may cause death of tissue in a very 
short time, either by the direct coagulating or carbonizing effect, or indirectly 
by the formation of thrombi in the vessels, or by paralytic action on the 
vessels of supply. 

3. Chemical Causes include the action of a fairly large number of sub¬ 
stances. Some authors include some of the bacterial toxins, although many 
of these would not properly belong here, if their action were understood. The 
action of tissue juices in the normal secretions and excretions may, however 
be included here, since they produce digestion necrosis. 

The most common chemical substances leading to gangrene are strong 
acids, hydrochloric, nitric, sulphuric, acetic, trichloracetic; also carbolic 
acid and lysol when applied as wet dressings. The secretions and excretions 
that bring about necrosis through their specific ferments are gastric juice 
escaping through a gastric fistula, extravasated urine, and the feces. 

4. Microbic Agents, certain virulent bacteria, particularly in the presence 
of intense traumatism, may bring about a combination of infection and 
gangrene often called microbic gangrene. 

The toxins produced in bacterial inflammation are also regarded as being 
responsible for destruction of tissue, or even for gangrene. 

B. Internal or Indirect Causes.— Injury of the main nutrient vessels may 
be brought about by mechanical force in several ways, as when a limb is 
crushed or receives an intensive trauma, when a large vessel is pierced by a 
gun-shot, when pressure effects are produced by an aneurysm or a malignant 
tumor, then the circulation may be impaired indirectly, through interference 
with the continuity or patency of the chief nutrient vessels. Ligation of a 
vessel, such as the spermatic artery during an operation upon the testicle, or 
for hernia, or ligation of a renal or middle colic artery, may lead to necrosis and 
gangrene. Ligation of the internal carotid artery is followed by necroses of the 


CLASSIFICATION OF GANGRENE 


161 


brain, in almost 50 per cent of the cases. In the case of the extremities, liga¬ 
tion of one of the main arteries may be followed by gangrene if adequate 
collateral circulation does not become established. The general condition of 
the patient, the heart action, the presence of complicating diseases (such as 
anemia, diabetes, infections and atherosclerosis), of inflammatory conditions, 
exudates or hematomata in the affected limb, and tight bandages—are all 
contributary causes that hinder the establishment of collateral circulation. 

Diseases of the blood vessels including first ather0- or arteriosclerosis (senile, 
presenile, diabetic, with or without thrombosis and embolism); second 
thrombo-angiitis obliterans; and, third, endarteritis (•including syphilitic endar¬ 
teritis) ; and fourth, acute arteritis and miscellaneous affections. 

Thrombosis or Embolism. —Complete obliteration of the lumina of either 
normal or diseased vessels through thrombi or emboli may lead to gangrene. 
When these occur in diseased vessels, they may be regarded as compli¬ 
cations of the primary vascular lesion. Therefore only such obturation in 
vessels relatively patent will be discussed under this caption. 

Emboli and thrombi may be composed of red clot, mixed clot, bacteria, 
purulent or even tumor material. For practical purposes we need consider 
merely clots; other embolic material more frequently evokes small areas 
of necrosis, suppuration or aneurysm, than true gangrene. 

Embolism most frequently affects the femoral or popliteal artery and may 
then result in gangrene of the foot and leg. More rarely the brachial and 
axillary arteries are involved. It occurs most commonly in the course of 
severe infectious diseases, or as a complication after the disease has subsided, 
also with valvular heart lesions, and after abdominal or pelvic (particularly 
gynecological) operations. In typhoid fever, pneumonia and influenza, 
sudden blockage of the popliteal or femoral artery may occur, or there may be 
extensive thrombosis of the femoral vein. Although it is not generally 
understood why an embolus in the popliteal artery should cause extensive 
gangrene, when there are adequate avenues of blood supply through collaterals, 
the explanation is often to be found in the fact that extensive red thrombosis 
is soon superadded above and below the site of the orignal clot, red and mixed 
thrombi extending in both directions with great rapidity into many of the 
smaller vascular branches and tributaries, preventing in this way the estab¬ 
lishment of a subsidiary collateral circulation. 

C. Neuropathic Gangrene.—In this group may be placed all those cases 
in which the arteries and veins are organically intact, or have suffered 
no alteration of their patency, and in which, in the present state of our 
knowledge, we assume that a neurogenic causal agency is responsible. 

The following symptom-complexes, Raynaud’s disease, erythromelalgia, 
acroparesthesia, multiple neurotic gangrene, and chronic acro-asphyxia be¬ 
long here. It has been generally accepted that in some of these, the vascular 
disturbances and arrest of circulation may be accounted for on the theory of a 
spastic condition of the nutrient vessels, but in others, the true mechanism 
still remains unrecognized. 

The various clinical forms of gangrene will be grouped and described 
according to the following classification: 

I. Gangrene due to external or direct causes, viz.: 

A. Trauma. 

B. Thermal influences . 

C. Chemical causes. 

D. Microbic action. 


n 


162 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


II. Gangrene due to indirect or internal causes, including 

A. Injury to main nutrient vessel of a part. 

B. Diseases of blood vessels. 

1. Arteriosclerosis. 

2. Thrombo-angiitis obliterans. 

3. Endarteritis {luetic). 

4. Miscellaneous arterial affections. 

C. Thrombosis and embolism. 

III. Neuropathic gangrene. 


CHAPTER XXIX 

CLINICAL EXAMINATION IN GANGRENE 

Examination in Prodromal Stages. —In order to understand and give the 
proper dignity to all of those clinical manifestations that constitute the 
prodromal signs of symptom-complexes that eventuate in gangrene, it is 
wise to follow a certain scheme of procedure in the examination of all cases 
in which we suspect impaired circulation. When we are confronted 
with cases of vasomotor disturbance, of trophic disorder, such as ulcers 
and atrophy, when the patient complains of pain which arouses the sus¬ 
picion of intermittent claudication, as well as in the presence of true gangrene 
of the lower extremities, the following method of the author will be found 
of value in diagnosis. It includes the investigation of the following points: 
First, the general appearance of the limb in the horizontal position; second, 
in the dependent position; third, the presence or absence of ischemia in 
the elevated position; fourth, the estimation of the angle of circulatory 
sufficiency ; fifth, pulsation in the palpable vessels, iliac, femoral, popliteal, 
posterior tibial, anterior tibial and dorsalis pedis in the case of the lower 
extremities, radial, ulnar, brachial and axillary in the upper extremities; and, 
sixth, the occurrence of induced , reactionary rubor or erythromelia. The 
value of nerve status need hardly be emphasized. 

1. General Appearance of the Limb .—Any departure from the normal should 
be noticed, such as the presence of fissures, ulcers, perforating ulcers, bullae, 
ecchymoses, impaired nail growth, gangrenous areas, distinct gangrene, 
signs of infection or lymphangitis or venous thrombosis. Evidences of 
malnutrition, such as atrophy, exceptional prominence of the bony landmarks 
and extensor tendons, conservation or effacement of the normal irregularities 
of contour through edema or through thickening of the skin and subcutaneous 
tissues, are features of importance. Variations from the normal color—partic¬ 
ularly marked pallor in the horizontal position, a play of color over the foot, 
even in the horizontal position; cyanosis, increased redness—all these, are 
manifestations of either impaired circulation or vasomotor disturbance. 

2. Rubor or Erythromelia .—With the foot in the pendent position and in 
the absence of inflammation, a red flush involving the toes and dorsum, as 
well as sole of the foot, extending upward for a variable distance, rarely 
farther than the ankle, is a phenomenon that is characteristic of many cases 
and many types of reduced circulation due to vascular obturation. This is a 


CLINICAL EXAMINATION IN GANGRENE 


163 


condition of rubor or erythromelia 1 (Gr. erythros- red, melia- limb). It is 
brought about by a compensatory dilatation of the superficial capillaries, and 
is most characteristic of the disease, thrombo-angiitis obliterans, although 
also found in other arterial affections attended with closure of larger vessels. 
It is frequently present in arteriosclerotic and diabetic cases as well. It 
seems to be an effort on the part of nature to make up for the impairment of 
circulation by virtue of dilatation and engorgement of the superficial capil¬ 
laries. Although more striking in the pendent position, the rubor may also 
be present in the horizontal position, and when continuously in evidence, 
may be termed chronic rubor, chronic erythromelia , in contra-distinction to the 
reactionary rubor that may be induced by depressing the limb after previous 
elevation. These terms, erythromelia, chronic rubor, reactionary rubor, 
induced rubor, angle of circulatory sufficiency, as well as others employed 
here, have been adopted by the author in an attempt to facilitate expression 
of various conditions of circulation, and if adopted, must be carefully applied 
in the sense here suggested. 

3. Ischemia or Blanching. —This usually sets in rapidly when the affected 
limb is elevated, whenever mechanical interference with the circulation is 
present. The extent of the blanching and the rapidity with which it 
appears, are both valuable aids in the estimation of the amount of obstruc¬ 
tive arterial disease. When the affected limb is cold, the tips of the toes 
may remain slightly blue or cyanotic. Should the blanching be slow in 
appearing, or very hard to determine, pressure upon the tips of the toes 
after the limb has been elevated for some time will demonstrate whether the 
part has become depleted of blood or not. Before elevation, pressure over 
the toes will cause an anemic area in which the color returns tardily 
(Expression test). Compression of the toes of the elevated foot in normal 
cases will reveal the presence of sufficient bright arterial blood (rarely 
slightly cyanotic), whilst a varying degree of ischemia, with or without 
marked cyanosis will accompany obliterated or obstructed arteries. 

4. The Angle of Circulatory Sufficiency (Fig. 43).—The estimation of this 
angle is based on the supposition that the normal limb, when elevated so as 
to be perpendicular to the horizontal plane, that is 180°, still retains most of 
its color. When the circulatory mechanism is defective, and the limb is 
elevated to the vertical, a variable degree of blanching of the foot occurs. If 
the leg is then gradually depressed, the angle at which a reddish hue returns 
(angle of circulatory sufficiency) will be found to vary considerably. In some 
cases it will be necessary to depress the limb to the horizontal before evidences 
of return circulation are manifest. The angle of circulatory sufficiency would 
then be 90°. If the reestablishment of visible circulation in the skin neces¬ 
sitates depression below the horizontal, the angle will be correspondingly 
less than 90°. In many cases of arterial disease, the estimation of this angle 
is a valuable adjuvant, not only in the recognition of the extent of the circu¬ 
latory disturbance, but also in prognosis. 

When the deficiency in color of the foot appears but slight or doubtful, it 
is well to examine the sole of the foot flexed at right angles with the patient in 
the prone position. The difference in the color of the two feet may thus 
become more apparent. When infection is present, tenderness over the 
plantar region will often be elicited, and indicate deep necrosis or suppuration 
complicating a gangrenous digit, even though no superficial sign thereof— 
such as redness—be in evidence. 

1 Not to be confused with “Erythromelia” a term used by Pick to designate an atrophic 
cutaneous malady. 


164 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Vasomotor symptoms may interfere with the estimation of the angle, of 
circulatory sufficiency. Sometimes the blanching of the foot together with 
the cyanosis induced after elevation may remain so long, that the angle can¬ 
not be determined. In these cases it is not the obstruction of the vessels, 
but the special vasomotor irritability that is responsible for the lack of usual 
reactive hyperemic response; for, neither is it constant, nor does it regularly 
interfere with the test. Such vasoconstriction is also not always present to 
the same degree. It is, therefore, incumbent upon us to apply the test on 
several occasions, to preclude the fallacies that vasomotor lability may 
occasion. 


180 ° 



Fig. 43.—Method of determining the angle of circulatory sufficiency. 


By a comparison of the circulation of both lower limbs, valuable informa¬ 
tion can be gleaned as to the degree of involvement of the arteries in each, 
also in the corroboration of a presumptive diagnosis of obliterated arteries in 
the limb that gives no subjective symptoms. 

So it may be necessary to depress one limb from 180 to 90° (horizontal) 
in order to effect a return of color into the toes, whilst in the other, a complete 
blush occurs at 135° (45 0 more elevated). The circulation may show visible 
advance up to a certain point (such as the base of the toes) at one angle, and 
still greater pendency may be required to promote a flux into the toes. These 
or even more of the foot may remain cadaveric in hue until the horizontal or 
possibly a lower position is reached. 

5. Absence of Pulsation as an Indication of Arterial Occlusion .—We should 
be able to feel the femoral, posterior tibial, popliteal, and dorsalis pedis 
arteries, pulsating in almost all individuals who possess patent arteries. 
In rare cases the dorsalis pedis may be aberrant in its course, and there- 














CLINICAL EXAMINATION IN GANGRENE 


165 


fore not palpable in its usual situation, or, neither the dorsalis pedis nor 
popliteal may be accessible to the touch because of the stoutness of the 
patient. 

To palpate the popliteal satisfactorily, the patient is placed on his abdomen, 
lying prone. The leg is held at right angle, that is, vertical, the patient being 
asked to relax the hamstring muscles. The artery is then sought in the upper 
half of the popliteal space, just outside of the semimembranosus and 
semitendinosus tendons (Fig. 42), the fingers being pressed downward against 
the femur. In the upper extremities, the radial, ulnar and brachial and 
axillary arteries should be examined for pulsation. 1 

The absence of pulsation is as a rule, an indication of occlusion at the point 
palpated, although in some instances dissections have shown that the site of 
obliteration is somewhat higher up. 

6. Reactionary Hyperemia , Rubor or Reactionary Erythromelia. —By this 
term we mean an induced rubor that manifests itself in the dependent position 
of the foot, after it has been previously elevated to the vertical. It is a physio¬ 
logical phenomenon, that ischemia or blanching of a limb artificially produced 
by an Esmarch or Martin bandage, will be followed by sudden dilatation of the 
capillaries of the peripheral parts, when the circulation is allowed to return. 
So, also blanching will occur in a leg whose larger arteries are occluded , on mere 
elevation from 60 to 90° above the horizontal , without the use of any artificial 
means. When such a blanched limb is then depressed to the pendent posi¬ 
tion, a similar induced or reactionary rubor will become manifest. This well- 
known manifestation may be invoked in the examination of cases in which 
impaired circulation due to arterial occlusion is suspected. It will be found 
particularly useful in cases of thrombo-angiitis obliterans, although also 
demonstrable in other cases of organic vascular disease. In early cases, it is 
a particularly valuable sign, for it may be present long before the chronic 
condition of rubor or erythromelia develops. 

It is a manifestation analogous to the hyperemia (Bier) induced by the 
application of an Esmarch or similar bandage or tourniquet to a limb, imme¬ 
diately after the arterial compression is removed. 

In a sense all chronic rubor of the pendent position is a reactionary rubor , 
when it accompanies obstructive arterial disease. For, is there not always 
a relative ischemia of the peripheral parts; and is not this brought about in 
varying degrees by every elevation of the limb, even if only to the horizontal? 
Indeed, it will be elsewhere shown (page 238) that in cases of marked 
impairment of the peripheral circulation, the foot is already blanched 
in the horizontal position, or even when flexed slightly below this level. 

Tests for Circulation.—It is indeed desirable to possess a sign, criterion or 
symptom that would afford a measure of the circulatory intensity of the leg, 
above the usually gangrenous parts of the foot. Search has been made for 
single phenomena that might fulfill this desideratum and a number of tests 
have been evolved. Among these may be mentioned those of Moskowicz, 
Matas and the author. 

We shall refer later to the limitations of such evaluations and to the impor¬ 
tance of that incommensurable and inestimable factor—the excessive demands 
for healing. For, when investigations of the degree of force and extent of 
collateral circulations are practically applied, they have been regarded by many 
authors as especially valuable in determining the lower safe limit for amputa¬ 
tion. In our own experience, all such tests are more reliable in fore-telling 


1 Some of the anomalies of the radial and ulnar arteries are mentioned in Chap. II. 


166 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the probabilities of the healing of the trophic disorders, or in fore-casting 
the advent of gangrene, than in setting indications for the site of operation. 

The Moskowicz Test} —This depends on the phenomenon that soon after 
removing an elastic bandage that has set the circulation of a limb in abeyance, 
an active hyperemia replaces the cadaveric hue. This striking rubor begins at 
and is sharply demarcated above, at the level of the constrictor. Thence it 
extends rapidly, down the extremity (peripherally) till it reaches the tips of the 
toes or fingers. 

After holding the extremity high for a short time (and this concerns 
especially the lower) an elastic bandage is firmly applied as far up as pos¬ 
sible and allowed to remain for 5 minutes. After removal of the constrictor, a 
prompt hyperemic blush is to be expected, when the circulation is adequate. 
When vascular obturation exists, the reaction is weaker and the extension of 
the blush towards the distal parts is slow. Often ischemic islands in the 
skin seem to tarry for some time, and in some instances a marmorated appear¬ 
ance will be prolonged. The hyperemia may progress rapidly to a certain 
level where its further spread is arrested or allowed to descend very slowly. 
In comparison with the less affected normal limb, the persistence of periph¬ 
eral pallor in the more diseased extremity will be found most striking. 

Moskowicz is of the opinion that the lower boundary of the hyperemic zone 
or point just above this, marks also the level of the obturation of the arteries. 
Reasoning thus, he sets the indications for the proper niveau for operation 
by selecting a level within the area of reactionary rubor—namely a short 
distance above its peripheral limitations. 

In our own experience this test is unreliable. Indeed, certain dogmatic 
and arbitrary rules that we have adopted as the result of a multitude of 
clinical observations are to be followed, in the selection of the level for ampu¬ 
tation, rather than teachings such as the above. 

The Matas Test*— This is a modification of the Moskowicz test for 
estimating circulatory sufficiency in cases of aneurysm. Although the pur¬ 
pose and technic of the Matas method are somewhat different from that of 
the latter, they are similar in utilizing the hyperemic blush following arti¬ 
ficial ischemia to determine the limits of adequate circulation. The principle 
according to which this test is employed is based on the fact that whilst the 
main arterial trunk is compressed in close proximity to the lesion (wound, 
aneurysm, tumor) sufficiently to arrest pedal pulses or fill an aneurysm, the 
collateral distribution is allowed to give evidence of its extent and magnitude. 

This segregation of the visible signs of collateral from those of the normal 
circulation is obtainable by excluding the main artery as a factor through com¬ 
pression, simultaneously with the abolishment of all impediments to arterial 
flow through other channels. 

An elastic bandage, after preliminary elevation, is applied from the digits 
to the level of the lesion, usually the aneurysm, after which a compressor is 
applied to the artery above the aneurysm. The elastic bandage remains in 
situ for 10 minutes in the young, 5 to 6 minutes in the aged, and is then 
removed, whilst the main artery is completely occluded. Immediately upon 
removal of the bandage, a hyperemic blush descends downward rapidly, 
progresses onward to variable extent, in proportion to the development of the 
collateral circulation. More often, the hyperemia may stop at a distance of 5 
or 6 inches from the compressor, or about 34 distance down the limb, then 

1 Moskowicz, L., Mitt. d. Grenzgeb. d. Med. 11. Chir., Vol. XVII, p. 216. 

2 Matas, Jour. Am. Med. Assn., 1914, p. 1441. 


CLINICAL EXAMINATION IN GANGRENE 


167 


continuing in a subdued color, traveling towards the periphery, but the 
extreme end of the limb, foot, or hand retains a cadaveric waxy pallor for 
several seconds or even 40 minutes, according to the development of 
collaterals. Then this waxy color gives way to a pale living color. Where 
collaterals are well developed, the hyperemic wave spreads in a few seconds, 
as if the artery had never been compressed. 

Matas in 1914 had used this test in 26 cases of aneurysm and other lesions, and the 
conclusions furnished by this test have been invariably confirmed by operative demonstra¬ 
tions and results. He used this test therapeutically in several cases, where the reaction 
was long delayed, for the purpose of increasing the collateral circulation, as follows. He 
postponed operations for days or weeks, in order to develop collateral circulation by system¬ 
atic compression of the main arteries, conjointly with dry hot air, baths and massage. 

Whilst the Matas and Moskowicz tests may have a sphere of applicability 
when a limited arterial territory suffers obturation, they are not very reliable 
in peripheral vascular disease. In thrombo-angiitis obliterans or marked 
arteriosclerotic disease of the vessels, certain elements of these tests would 
need modification. The application of an Esmarch bandage is not to be 
recommended in view of the deleterious effects of such intensive ischemia, 
and the direct mechanical lesions that might ensue. Furthermore, the periph¬ 
eral pulses are not usually palpable, and therefore no guidance. It has 
been the author’s custom to employ a method based on hydrostatic prin¬ 
ciples which has been previously described. In view of the extensive vascular 
obliteration that accompanies thrombo-angiitis obliterans, it is noteworthy 
that no great differences can be elicited at times, between the color reaction 
that follows the depression of the limb after prolonged elevation (gravity 
depletion), and that resulting after separate compression of a main artery. 
This is comprehensible when we consider that the very main vessel compressed 
may have become a negligible factor in the delivery of blood even through 
collaterals; and when we take into consideration the multitude of occluded 
branches emanating from this trunk. In other words, such main arteries 
are not essential to complete the collateral circuit and the latter depends on 
even more remote and deeper channels and anastomoses. 

Allan and Matas have also experimented with the occlusion of the main artery by flat 
and pliable aluminum bands. Such a band is applied about the vessel supplying the part 
to be tested. If the collateral circulation is adequate, the band is left in place, and becomes 
encysted in the tissues. If gangrene threatens, the band is made more lax, so as to facilitate 
a better collateral circulation. The bands are made long and narrow so as to pass through 
aneurysm needles. After such a band encircles the vessel, it is tightened with the fingers 
until the pulse is obliterated distal to it. 

Value of Tests for Circulation in Thrombo-angiitis Obliterans .—The 
Moskowicz test according to some authors is of value in determining the safe 
point to amputate in presenile and in senile gangrene. Matas cites examples 
in which he was successful in recognizing that amputation could be performed 
below the knee, because the hyperemic blush extended well below this level, 
thus indicating that a flap would be viable. 

The author’s experience in cases of thrombo-angiitis obliterans has con¬ 
vinced him that, although the test may demonstrate to what extent a 
collateral circulation has become established or even how far a compensatory 
hyperemic state has been developed, it does not, with any degree of precision 
or reliability, denote where amputation should be carried out. This is true 
because it cannot correctly gauge the likelihood of healing after an incision 
is made, even though it demonstrates the centrifugal limit of collateral skin 
circulation. For, it must be remembered, that not only is it necessary to 


168 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


have blood enter the most peripheral parts after amputation, but nature 
makes excessive demands for purposes of healing. The exigencies evoked 
by the new conditions may be incommensurate with, and far exceed those 
hydrostatic factors that are sufficient to give a red color to the part. Not 
infrequently has gangrene of the flaps and other tissues at the point of 
ablation been observed when the Moskowicz test indicated ample collateral 
paths. Even when healing of the greater part of the wound does occur, an 
ulcer may remain at the point of drainage. This is then wont to enlarge and 
gives rise to gangrene or phlegmon formation. 

In short, experience in thrombo-angiitis teaches that an indication for 
amputation below the knee or below the level of the Gritti-Stokes method, set 
according to tests, is of theoretical rather than of practical value. In arterio¬ 
sclerosis amputation below the knee is also unreliable, although in rare cases 
it may be attended with good results. 

Henle-Coenen Method .—Almost simultaneously Henle, Lexer, v. Frisch 
and Coenen recorded an observation which they regard of value in estimating 
the degree of collateral circulation. It was applied by these authors to the 
treatment of aneurysms by ligation. In their judgment, indication for ligation 
would depend upon the positive result of the test. If a larger artery be 
sectioned transversely, not only the central but the peripheral stump should 
bleed copiously in a strong stream (Positive test). 

It is based on the fact that in many arterial territories (external carotid, 
arteries of the hand and foot), the normal collateral circulation suffices to 
give a copious reflux when the centrifugal current is interrupted at any point. 

Tests for the Patency of the Veins .—Whereas it is a relatively easy matter 
to determine with a fair degree of certainty whether the patient possesses 
patent superficial veins, the question as to the involvement of the deep veins is 
a most puzzling one. Thrombotic lesions in the palpable veins are des¬ 
cribed in detail in Chap. LVIII. In these latter cases one can watch the 
recurrences of thrombophlebitis throughout the thigh and leg and find it 
extending even to the sole of the foot. And, when personal observations 
are not at hand, anamnestic data may be forthcoming. 

What signs and symptoms are of value in indicating the patency or 
occlusion of the deep veins? It is here that we have to concede the inade¬ 
quacy of our clinical methods. In looking over the histories of the cases 
in which amputation revealed marked obliteration of the deep veins, only 
in very few was there mention of marked cyanosis in the pendent position 
of the limb. Whilst an unusual intensity and rapid advent of cyanosis after 
rubor may be a serviceable sign in this connection, it is not absolutely depend¬ 
able since vasomotor agencies play an important role in the determination 
of color phenomena. Inadequate vis a tergo and constricted arterioles in a 
pendent limb may suffice to give cyanosis without obstructive lesions of 
the veins. 


CHAPTER XXX 

TRAUMATIC GANGRENE 

Traumatic gangrene results from the direct action of a mechanical force. 
A rapid and direct disorganization of tissue may follow mechanical insults 
such as contusion, crushing, machine injury, injury through blunt force, and 



TRA UMA TIC GA NGRENE 


169 


pressure. The latter force acts in the main by interference with circulation. 
Tissue which has become totally separated must needs become necrotic or 
gangrenous, if the conditions for healing and restitution of the circulation in 
the wound are not favorable. Such adverse conditons arise when severe 
traumata bring about crushing and mangling of tissue, extravasations of blood 
and bacterial infection. Only in the case of transplantation by operation under 
strictest aseptic conditions, are the conditions favorable for restitution and 
growth of the transplant. 

A blunt crushing force may also lead to gangrene of tissue, partly by reason 
of the disintegrating and destructive action of the force itself, and partly 
through thrombosis in larger vessels. The severe traumata inflicted in 
various accidents by machinery, which produce extensive laceration of tissues, 
may be followed by gangrene of a part or the whole of an extremity. 

We may distinguish a number of varieties. Through separation of con¬ 
tinuity a mass of tissue may be detached and become necrotic, its attachment 
and healing being prevented by hemorrhage and infection, or through dis¬ 
placement of tissue elements (Decollement) and distortion, a blunt force 
leading to the formation of a subcutaneous pocket. Blood then fills this 
space; thrombosis of the torn and squeezed vessels takes place, and gangrene 
and necrosis are expedited. Or, ligations of vessels may lead to a similar 
issue, whenever the chances for the establishment of collateral circulation are 
slight. 

Observations on the results of traumata during the Great War have 
awakened interest in the indirect effects of trauma. Through the stimulation 
of the vessel nerves, contraction and later dilatation of the smaller blood 
vessels occurs. Intense trauma may evoke dilatation and finally complete 
vascular paresis with stasis and diapedesis. An ischemic necrosis of muscle 
is described as due rather to the implication of nerves, spastic contraction of 
vessels, dilatation and stasis, than as the result of direct forces. 

Finally, injuries leading to rupture and consequent ligation of larger 
vessels are not infrequently complicated by gangrene. Such an eventuality 
may be expected, when extensive hemorrhagic extravasations are present. 

Symptoms. Manifestations of threatened gangrene of an extremity begin 
with the picture of ischemia or venous stasis, coldness, and absence of pul* 
sations in the usually palpable arteries. After initial paresthesiae, or dull 
pain, complete absence of sensation and motor paralysis set in. Intense pain 
and tenderness, however, may persist above the area of gangrene. Within 
forty-eight hours, the evidences of beginning dry or moist gangrene make their 
appearance. 

It would be possible, although not fruitful, to make groupings according 
to the nature of the injury, its extent, whether the main arteries of a limb 
are implicated, as to whether the issue be gangrene of part or whole of a 
member, or merely limited necroses. 

The following classification although not all-embracing has some clinical 
value. 

1. Gangrene of limited extent involving larger or smaller areas of the 
integument, possibly attended with injuries (fractures or dislocations) of 
deeper parts. 

2. Gangrene of part of an extremity, usually the lower, due to direct- 
compressing forces with or without complicating thrombosis of the main 
artery; and 

3. Gangrene of almost the whole of an extremity (usually the lower). 
The most striking and characteristic examples of this variety are those 


170 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


severe injuries resulting from accidental entombment, so frequently observed 
during the Great War. . . 

1. Gangrene of limited extent requires no detailed description. When¬ 
ever a limb is subjected to such compressive or percussive force that the 
vitality of the tissues is compromised, local necrosis ensues.. When such 
devitalization with subsequent sequestration of slough is of limited extent, 
we usually speak of a “decubitus.” This may occur after the application 
of too tight bandages, or after even slighter insults in those in whom neuro¬ 
trophic and functional derangements already exist. More severe injuries, 
such as compressing, sliding and crushing forces against the extremities may 
result in more extensive death of tissue. These are seen in automobile, 
railroad and “ shoot-the-chutes” accidents, where the living force and 
momentum cause an extraordinary degree of local stress when resistance 
is encountered. Even gangrene of a part or the whole of a limb may eventu¬ 
ate, especially if the main artery be traumatized and thrombosed. 

2. Gangrene of an Extremity. —Traumatic gangrene of the lower extrem¬ 
ity is best exemplified by that resulting from accidental entombment. The 
cases may be grouped into: 

A. Gangrene with, and 

B. Gangrene without blockage of the main arteries. 

3. Accidental entombment, formerly of rare occurrence and rarely seen 
except in mining and building operations or earthquake, was not infrequently 
the cause of extensive gangrene of the extremities during the Great War. 
The injury to the extremities following such trauma is attributable to 
external pressure and is characterized by the absence of external wounds, 
the absence of severe external contusion, and of infection. 

Similar injuries have been described as occurring during earthquakes 
and Colmers 1 reports acute decubitus as the result of such injury. The 
contusing force acts for many minutes or hours by reason of the fact that 
the injured person is imprisoned and incarcerated under earth, stone, debris, 
etc. Gangrene of a portion or the whole of the extremity, resulting from 
such a trauma is characterized by the absence of external wounds and of 
infection. 

Acute traumatic decubitus is a condition resulting from incarceration of 
the body or entombment for many hours, the compressing forces bringing 
about localized gangrene. The skin, the soft parts, as well as the bones may 
become involved. Strange to say the integument may remain intact, whilst 
the fascia and muscles become necrotic. Subsequently infection leads to 
extensive phlegmon formation. The gluteal and trochanteric regions are 
the sites of predilection. After sequestration of the dead tissue, large 
punched out holes or cavities are left behind (Colmers). 

A. Gangrene with Arterial Thrombosis. —The trauma is usually exerted 
over the thigh. The symptoms include rapid development of necrosis of 
the lower extremity without the presence of any wound or an infectious 
process. The lower extremity becomes enormously swollen, tense and 
indurated; the skin of the whole leg is discolored, has a livid hue, is mar- 
morated with areas of pallor, sometimes with superficial excoriations. The 
whole limb is immobile and cold up to the knee or even higher. The pulses 
in the dorsalis pedis and popliteal are usually absent. 

If the patient is not already in shock, the usual symptoms of the latter 
develop, and exitus occurs in most of the cases within a few days after the 
injury. 

1 Colmers, Arch. f. klin. Chir., 1909, 90, p. 703. 


TRAUMATIC GANGRENE 


171 


The femoral artery at the site of the greatest compression may be throm¬ 
bosed, the intima injured and detached, or the seat of suggillations. Second¬ 
ary thrombosis in the femoral vein develops later, and may contribute to 
the development of gangrene. 

B. Gangrene Without Involvement of the Main Arteries. —Here we may 
distinguish gangrene of the leg with mortification of (i) the superficial 
tissues, or (2) the deep tissues. 

1. Traumatic Superficial Gangrene with the Main Vessels Intact. —This 
variety is characterized by the fact that but a short time after release from 
entombment the picture of impending gangrene rapidly develops. The leg 
may be markedly swollen, cold and tense, the peripheral pulses absent. 
Changes in the appearance of the skin are striking in that the color is first 
bluish red and marmorated in places. Soon there develop large vesicles 
or bullae partly filled with light colored fluid or blood. Signs of infection 
are usually absent. Shock is associated only in the cases sustaining severe 
trauma, but local pain may be severe. With the progress of the gangrenous 
process, temperature is common and amputation becomes indicated. 

The cause of the tissue death seems to be the force of external pressure. 
Whilst complete mortification may involve all of the tissue lying upon the 
deep fascia, the underlying parts are the seat of hemorrhagic infarction and 
thrombosis of the smaller vessels. In spite of the fact that the vitality of 
the deeper tissues is not altogether compromised, their integrity and future 
outlook gives little promise of functional restoration. In spite, therefore, of 
only superficial necrosis, amputation usually becomes necessary. 

Pathology. —The skin of the leg is usually extensively infiltrated with 
blood and the veins thrombosed. The subcutaneous tissues, too, show 
brownish black discoloration with numerous thrombosed vessels. As for 
the tissue under the fascia, the muscles may show but slight changes save for 
some hemorrhages. Except for some bloody extravasation, piossibly bony 
fractures, all of the deeper tissues may escape the destructive mortifying 
process. 

2. Traumatic Gangrene of the Deep Tissues (with main arteries intact).— 
Although the limb will here also give early evidences of interference with its 
nutrition, gangrene develops more slowly. Indeed, months may elapse 
before amputation seems warranted. The circulation of the skin may 
appear unimpaired for some time (Orth 1 ); or coldness and pallor may be 
present (Kuttner 2 ) from the beginning. 

The characteristic feature of this variety of traumatic necrosis is the dis¬ 
turbed nutrition of the musculature and the intensive swelling of the deeper 
tissues, the skin and subcutaneous tissue suffering relatively little. The 
latter may, however, become secondarily involved. Gangrene of the 
extremity does not necessarily follow especially if no secondary infection 
supervenes. Or the muscle alterations may subside if not too severe. In 
these circumstances function may become restored, or more or less perma¬ 
nently impaired. 

In short, primary necrosis of muscles is believed to occur in these cases. 
Prolonged action of an equally distributed contusing, compressing force 
may explain the involvement of muscle and escape of the integument, in 
contradistinction to the more intensive stresses that bring about mortifica¬ 
tion of the skin. 

1 Orth, Miinchen. med. Wchnschr., 1916, No. 39, Feldarz. Beilage, No. 39, p. 1407 

2 Kuttner, Bruns’ Beitr., 112, 1918, p. 591. 


172 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

Treatment— The treatment of traumatic gangrene includes first, the 
surgical treatment of the wound produced by the injury, according to the 
principles of aseptic surgery; second, the methods for enhancing the circu¬ 
lation, so as to limit the gangrenous process, as much as possible; and third, 
the amputation of the affected part. These methods will be given due 
consideration in Chap. LXV. 


CHAPTER XXXI 

THERMIC GANGRENE 

Intense heat or cold may bring about necrosis of tissues within a very 
short time, while a moderate degree of heat and cold may have the same effect 
when in action for longer periods. Gangrene from cold apparently differs 
in no essentials from other forms of mortification. The death of tissue may 
occur first, from the direct action of cold upon the protoplasm; second, from the 
ischemia due to vascular spasm; and third, thrombosis. Although gangrene 
may be due to the fact that the part has become completely frozen, restitution 
would occur in most instances were it not for the fact that extensive thrombosis 
of the arterial and venous channels has already occurred. 

For a thorough understanding of the gangrenous processes depending 
upon the action of cold, it is well to have some knowledge of the observations 
that have been made on the effects of such influences during exposure in time 
of war. It was during the recent Great War that a multitude of lesions depen¬ 
dent upon exposure to cold and moisture developed, many of which were 
accompanied by gangrene. 

General Consideration. —In studying the effect of cold on human tissues 
we must take into consideration both the local and the general action. The 
human organism can adopt itself to very marked diminution in the surround¬ 
ing temperature, without any considerable loss of body temperature. The 
body compensates for loss of warmth by increased heat production. So 
important is the matter of tissue nutrition that in the absence of an ade¬ 
quate delivery of blood the body warmth may be reduced to a degree incom¬ 
patible with a continuance of the vital functions. The consequences of 
the local action of cold on the tissues vary according to the degree of tem¬ 
perature, the duration of the action, and the character of the environmental 
circumstances. 

Cold, dry air has an effect different from cold water or snow, whilst the 
effect of air in motion is notably at variance from that of an absolutely tran¬ 
quil atmosphere. These variations are due in part to the fact that loss of 
body warmth to the air is effected through radiation, whilst the physical 
process is one of conduction in a watery, humid, or moist medium. The 
red blood cells are said to be destroyed through freezing. Lesser degrees of 
cold produce primarily a constriction of the vessels, first of the smaller then 
of the larger arteries. The pain due to cold results from the direct action of 
loss of warmth upon the sensitive nerve endings. Consequent upon vaso¬ 
constriction comes vasodilatation, when the temperature rises; and redness 
and cyanosis of the exposed part ensue. 



THERMIC GANGRENE 


173 


A wet cold is especially apt to bring about marked redness and swelling 
of the part, in anemic individuals. Such individuals easily develop chil¬ 
blains (pernio). The protracted action of moderate degrees of cold (not 
approaching the freezing point) may so disturb the arterial circulation, as to 
produce ischemia of the peripheral parts—toes and fingers—and gangrene. 
This ischemic type of gangrene must be distinguished from the immediate 
and actual result of freezing of a part. 

Experimental work on the local lesions due to cold has produced a number 
of interesting lesions, among which may be noted the following; thromboses 
of the vessels (Hodara and Riehl); dehydration and ice formation in the 
tissues (Rischtler). 

Symptomatology of Local Freezing. —Freezing of the tissues may be 
divided into three types. First, simple freezing with erythema as the chief 
symptom (first degree chilblain); second, with formation of vesicles; third, 
with gangrene. A fourth type has been suggested by Florcken, 1 without 
skin lesions. 

It was found during the Great War, that robust and strong individuals, 
who had been exposed for a considerable period of time in wet trenches, or 
had worked in cold water, presented the following clinical picture. There 
was severe pain, stiffness in the legs and back, with inability to use the muscles. 
Muscles, tendons, periosteum and the shin bone, as well as nerves seemed to 
be tender to the touch without any palpatory lesions, without objective changes 
of sensibility or altered reflexes. The most frequent localization of these symp¬ 
toms was the region of the shin bone. Certain German authors have given 
the name “Schienbein Schmerz” to this syndrome. 

The result of exposure during the war sometimes gave clinical pictures 
simulating influenza, typhus, perityphus and other diseases. Thus, Sipp- 
mann described headache, chills, fever, malaise as preceding the attacks of 
pain. The relationship between the characteristic tibial pain, and the general 
symptoms has been a mooted question. There can be no doubt, however, 
but that the intense pain in the extremity can be brought in direct causal 
relationship with the exposure to cold. 

Local Changes Due to Cold. First Degree .—Portions of the body exposed 
to cold become reddened, whilst severe burning and prickling sensations are 
experienced (nerve irritation). As a result of vasoconstriction the parts 
become blanched and anesthetic. Rubbing of the parts may restore circu¬ 
lation. Following the vasoconstriction, intense reddening of the peripheral 
parts with itching and pricking sensation follows, the extremities becoming 
swollen. All of these symptoms my subside completely or lead to the develop¬ 
ment of chilblain. These are represented by bluish red, flat swellings, or 
nodular elevations surrounded by a red zone. The sites of predilection are 
the extensor aspects of the fingers and toes, the margin of the foot, the heel, 
the ball of the foot and the back of the hand. However, ears, nose, cheeks, 
and more rarely the penis, the gluteal region, and the chin may be affected. 

Second Degree .—Freezing of the second degree is characterized by the 
presence of bullae or vesicles on a reddened or violaceous skin. The con¬ 
tents of the vesicles differ from those of gangrenous vesicles in that there is 
clear fluid just as in the blebs of burns. After the bursting of the vesicles 
the superficial epithelial defects heal rapidly. In rare cases, however, ulcers 
may form that are of indolent character. Certain authors have brought these 
lesions into relationship with subsequent arterial changes eventuating in gan- 

1 Florcken, Ergebn. d. Chir. u. Orth., 1920, p. 185. 


174 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

grene (Von Winiwater). The particular disease, however, described by this 
and other investigators has been shown by the author to be none other than 

thrombo-angiitis obliterans. . . . , , 

Third Degree .—When the fingers or toes suddenly turn blackish and 
cannot be moved, lose their sensation and become cold as ice, we have the 
typical picture of this form. When the superficial portions have been dam¬ 
aged, then needle pricks and incisions are not experienced as pam, but on y 
merely as pressure sensations. Later, the affected parts become swollen, 
cyanotic, bluish-red and congested. If this circulatory stasis does not 
abate, then gangrene occurs. The fingers and toes may become totally gan¬ 
grenous whilst proximally merely the superficial tissue layers are involved. 

A rather characteristic type of gangrene is that involving the heel, and when 
this type is more extensive, the larger part of the sole of the foot becomes 
gangrenous. 

In certain instances, smaller or larger areas of skin and subcutaneous 
tissue of varying size over the shin bone, or in fact, over any portion of the 
leg may become frozen as the result of exposure in wet stockings or large 
indolent ulcers may result. , 

Clinical Course—The following clinical picture is described by Volk and 
Stiefler . 1 The affected extremity is swollen, exceedingly painful and 
temperature may accompany the local phenomena. The skin is livid and 
bluish and is lifted up here and there into large blebs or is easily cast off. 
Subsequently, extensive gangrene of the distal parts occurs, particularly 
when anesthesia has lasted for a few days. In the severe cases of freezing 
necrosis of the superficial tissues, involving muscles and tendons, and even 
mummification or moist gangrene of the fingers, toes or a portion of the foot 
may occur. Spontaneous amputation has been noted, and erosion into the 
large vessels may take place. Some authors 2 describe the occurrence of a 
moccasin-like gangrene involving the sole and big toe of the foot. 

Rather characteristic features are the implications of the heel, and the 
freezing of the finger tips without involvement of the thumb. Meyer and 
Kohlschiitter 3 describe typical pictures where the tips of all the fingers are 
frozen, ulcerate or become gangrenous, the thumb often remaining free. 

Regarding the symptoms of pain when parts are frozen, authors vary 
considerably. Zuckerkandl reports cases in which mortification of the 
affected part can occur without pain. Patients may have no knowledge of 
the state of the parts until, after removal of the shoes, the condition becomes 
manifest. In such cases spontaneous pain begins only then when the 
superficial blebs are opened, and the corium becomes exposed to the air. 
Other authors, such as Dreyer 4 report that in the moist gangrene observed 
during the Balkan war, pain appeared as a late symptom and was followed 
after seventy-two hours by swelling and gangrene. 

Still others have observed that practically all patients have subjective 
manifestations in the affected territory complaining of paresthesiae such as 
feeling of numbness, a wooden feeling, stiffness, prickling, formication, 
burning and sensations of heat and cold. 

About one-third of the cases under the observation of these authors 
developed, what they termed “ Erkaltungsneuralgie ” or neuralgia due to cold. 
This term was employed to designate a complex of pain in the feet, soles, and 

1 Volk and Stiefler, Wien. klin. Wchnschr., 1915, No. 5. 

2 Coenen, Thorn, Cilimbaris, Beitr. Kriegsheilkunde, Berlin, J. Springer, 1914- 

3Meyer and Kohlschiitter, Deutsch. Ztschr. f. Chir., Bd. 127, March 2, 1914. 

4 Dreyer, Zentralbl. f. Chir., 1913, Nr. 42. 


THERMIC GANGRENE 


175 


toes, with tenderness over the anterior tibial and perineal groups of muscles, 
manifestations that would subside after rest and the use of salicylates. When 
pain appears shortly or some time after the action of the cold, paresthesiae 
were often noted as prodromal signs; these were in no way related in inten¬ 
sity to the degree of the exciting process. Freezing of even moderate degree 
can evoke intensive paresthesiae. 

Quite in contrast to the sensory phenomena, in cases of ordinary gangrene, 
these authors observed derangement in sensation over much larger areas and 
extending much higher than was expected from the extent of tissue injury. 
Anesthesia may extend well above the line of demarcation (if gangrene occurs) 
and may be delimited above by a zone of hyperaesthesia. 

Etiology.—It is known that a reduction of temperature down to the 
freezing point of blood or below is not necessary to bring about what is 
known as freezing of the tissues; but that temperatures even above zero 
centigrade suffice provided that predisposing factors are at hand. Indeed 
gangrene may take place at a temperature considerably above the freezing 
point of blood (even 6° to 8° C.). 

Such predisposing factors are firstly, moisture (wetness); secondly, local; 
and thirdly, general predisposition, these including all the noxious factors 
that may lead to ischemia of the vessels. Whilst reduction of temperature 
of any part of the body through the action of cold air takes place by radiation, 
chilling of the body by reason of moist cold, such as wet clothing and snow, 
takes place more rapidly through direct conduction. The most dangerous 
degree of cold is at the thaw and melting point. It has been noted by Sticker 
that most cases of freezing during the Great War occurred during the time when 
the snow began to melt. 

Local predisposition is still further conducive. Thus, the distal parts of 
the body are most prone to become frozen, especially parts that are least 
well provided with blood. A disproportion between the surface extent and 
the volume of a part is another factor that makes fingers, toes and ears 
susceptible. 

Loss of heat is greater when the air is in motion. The presence of bodies of 
good conductivity, such as metal, is dangerous. Water, too, is to be feared 
when in direct contact with the skin. Those portions of the body which are 
not only exposed to cold, but suffer impairment of circulation through 
restricted motion, and constriction of the circulation are particularly sensitive 
to gangrene. The deleterious effects of tight shoes, shrunken and wet 
boots, and tight and wet stockings are well known. 

Internal causes are bodily weakness and disease. These minimize the 
body’s protecting forces. Lack of power of adaptation to surroundings 
is a predisposing cause. Thus, individuals who are able to withstand unusual 
climatic changes including exposure to moisture and cold are less susceptible 
to gangrene. A certain amount of resistance can be acquired gradually 
through artificial exercises. Statistics demonstrate that most cases of gangrene 
of this type occur in the autumn, whilst later in the season, when a certain 
degree of adaptation (acclimatization) has become possible, its incidence 
diminishes. 

Patients that have just recovered from a malady are also susceptible; 
which is in keeping with the frequency of gangrene in post-typhoid and in 
cholera cases. 

Pathogenesis. Direct Tissue Injury.—Tile is dependent upon the continu¬ 
ance of definite temperature in the protoplasm. There are upper as well as 
lower limits under which it can no longer continue. The lower limits vary 


176 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


considerably in different animals. In man and many of the warm blooded 
animals 25 0 C. is considered incompatible with existence. The circulating 
blood usually causes renewal of warmth. With impairment of circulatory 
activity, however, the two factors may combine to exert a deleterious result. 

The direct effect of cold, from the physical standpoint, is a change in 
the colloid solution of the protoplasm. Within certain limits it is rather 
the duration of the lowering of temperature than the degree that is impor¬ 
tant, so standing in cold water for many hours leads to gangrene, whilst 
freezing with the ethylchlorid spray for several seconds does not. It has 
been shown by Schade that the elasticity of the tissues may return to normal 
when the loss of warmth lasts but a short time. In addition to the changes 
in the colloids, chemical changes occur—changes in the crystalloid solution. 

The Effect of Freezing in This Type of Gangrene .—'The temperature of 
o° C. does not indicate a critical point. In vitro the blood and human fluid 
freeze at a temperature of — o.66° C. but in the body a much lower tem¬ 
perature is necessary. With the formation of ice, however, an additionally 
injurious factor is added. Freezing is only of significance in that a rapid 
and intensive loss of water is occasioned thereby. It is well known that 
plants that have been frozen show macroscopically and microscopically the 
same appearance as dried ones. Indeed, those forms of life that are not 
dependent upon water cannot die by reason of cold. 

Experiments have shown that with a marked lowering of temperature, an alteration 
of the protoplasma from the sol condition into the gel condition takes place; that is, the 
substances in solution approach the precipitate or solid state. JThe body cells do jiot 
possess the same characteristics or qualities at a temperature of 20° that they, do at 30 C. 
The microscopic examination, however, does not always show corresponding changes. 
The elasto-metric method of Schade is a new procedure for the investigation and demon¬ 
stration of this subject. In a specially constructed apparatus, this author showed that 
elasticity of the subcutaneous tissues diminished in a state of fatigue, general disease, 
and local cold, even though the fluid contents did not change. Elasticity is the quality 
or capacity for alteration of form and return to a previous state. A measureable loss, of 
elasticity can take place in fat-free tissues only through a change in the physical condition 
of tissues, namely, in their protein substances. 

After return to normal temperature, the disturbance in the colloid mixtures does not 
cease when the degree of what is known as “reversible” has been exceeded. 

The formation of ice in the tissues is another deleterious factor. As a matter of fact, 
the whole watery solution of colloids and crystalloids which we recognize as the fluid proto¬ 
plasm, the lymph and the blood plasma, does not become converted into ice. The ice forma¬ 
tion takes place in the precipitation or congealing of pure water in a solid form out of the 
tissues, with simultaneous concentration of the remaining solution. By virtue of the higher 
concentration of the colloids themselves, and particularly, the crystalloid substances, the 
tranference of the colloids into their gel condition is intensified. At the.same time carbon 
dioxid and oxygen previously held in by the water become free. The microscopic pictures 
noted in frozen ameba bear out this view. 

For the living cell therefore, freezing exerts its influence by virtue of a rapid and inten¬ 
sive withdrawal of water. And, furthermore, forms of life which we regard as latent, do 
not appear to suffer from cold. The time factor is important because the changes are slow. 
After a certain lapse of minutes, a portion of the cell protoplasm becomes converted into the 
gel condition so that the remainder does not suffice. 

The alterations in the protein substances are not reversible after long periods of freezing. 
This corresponds to the condition of frozen solutions of devitalized colloid substances, such 
as egg albumin which, even after being thawed, show their spongy structure, and do not 
return to their sol condition. These changes are the same for all degrees of temperature and 
the time required for annihilation of life varies. When the human skin is frozen with ethyl 
chlorid for from one to two minutes, it is assumed that during this period, an adequate 
portion of the protoplasm retains its sol condition, and can subsequently resume its vital 
function. Thus, some animals can withstand freezing for longer periods of time. It has 
been shown that medusae can remain frozen for hours. 

The manner of thawing does not seem to be as important as is believed. Clinically, 
acute gangrene does not ensue immediately after exposure to cold. The role of the blood 
vessels seems to be an important one. 


THERMIC GANGRENE 


111 


The Rdle of the Blood Vessels .—Authors are at variance, as to whether in 
gangrene due to cold (freezing) the reduction of temperature per se, or the 
cessation of circulation plays the greater role. Wieting 1 and Marchand 2 
have applied the word “ischemic” (Kalte-Gangran) to this variety. Accord¬ 
ing to this view the thermic influence produces a spastic contraction of the 
arteries, even to the extent of complete obliteration of their lumina. And 
because this effect may last for a considerable period of time, and other pre¬ 
disposing factors are at work, gangrene is the issue. Wieting believes that a 
vessel palsy together with true impairment of the vascular innervation, is an 
important activating factor, for with it go stasis and thrombosis. 

From what has been said it is clear that immediate action of withdrawal 
of heat from the protoplasm plays an important part in the production of 
gangrene due to cold, but it is not the only cause. The blood carries 
renewed calories to the refrigerated tissues, and it is only when the loss of 
heat preponderates over that which is received that injury to the tissues 
sets in. 

When the action of cold is very intensive, a deleterious result is obtained, 
even if the vascular system functionates with normal or accelerated activity. 

It is generally believed that contraction of the blood vessels follows stimulation by cold. 
If contraction of the vessels were the only and regular reaction on exposure to cold, the 
condition of gangrene due to cold would be adequately explained. Loss of warmth without 
substitution, absence of oxygen and nutrition would act similarly in bringing about cell 
death. 

Marchand 3 holds this view when he says that the anemia produced by contraction of the 
small vessels can become complete and can thus lead to death of affected parts. However, 
as a rule, the reaction of the blood vessels is somewhat more complicated. 

The first sequence of the action of cold water is, indeed, a contraction of all of the 
vessels in the affected parts, including arteries as well as capillaries and veins. The skin 
becomes pale and the extremities lose in volume. This condition may persist for some time 
in anemic individuals, the part remaining pale and cold, rigid, and permanent injury to the 
parts may ensue. In anemic people as a result of mere contraction of the blood vessels, 
death of tissue in the sense of an ischemic gangrene may eventuate. 

The cases in which gangrene occurs immediately after exposure to cold are 
telatively rare. Usually, days, weeks or months intervene before the injured 
rissues die off. Doubtlessly the condition of the blood vessels is responsible. 
To explain the delayed mortification, the question has been put as to 
whether the tissues are not found in a condition of diminished vital energy after 
the action of cold; also as to whether limited portions of tissues or cells can be 
injured or comparatively devitalized in the multicellular organisms and remain 
in such a state even after the causal agent has ceased to be active. Histo¬ 
logic and biologic observations, however, do not seem to lend acceptance to the 
view that single cells can remain in a state of permanent deterioration or 
devitalization, in a multicellular organism. Indeed, it seems rather more 
plausible that when such permanent or protracted local morbidity exists, 
lesions in the blood vessels are at fault. 

Animal experimentation has shown that the vessels may permanently contract as the 
result of the action of cold. When the extremities and ears of rabbits were put into a cold 
solution at 20° below o° C., they were found to remain bloodless until freezing took place. 
When the same cold mixture was brought into contact with the femoral arteries, so inten¬ 
sive a contraction was obtained, that no blood passed through it (Catiano 4 ). In healthy 
individuals and under atmospheric conditions in which adaption has taken place, a dilata- 

1 Wieting, Centralbl. f. Chir., 1913, p. 593. 

2 Marchand, Krehl-Marchand, Handb. d. allg. Path., 1908, 1, p. 114. 

3 Marchand, Handb. d. allg. Path., 1908, Bd. 1, also 1912, Bd. n. 

4 Catiano, Langenbecks Archiv., 1883, Bd. 28. 


12 


178 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


tion of the vessels follows sooner or later. Further investigation has shown that transitory 
reduction of temperature of an artery is followed by immediate contraction, but after a few 
minutes circulation is restored, and the vessel dilates beyond its original calibre. E ven when 
cold is applied for a longer period of time it is found that in the frog after preliminary 
vasoconstriction, dilatation takes place beyond the normal, and whilst the cold is still in 
action. After restoration of the external temperature, the vasodilatation^may continue 
for from ten to twenty minutes or more (Sartorius 1 ). In the case of the rabbit, too, when 
cold acts slowlv, excessive dilatation may occur after preliminary contraction and persist 
for many hours', even though the snow be still in contact. It is believed that this reaction 
of vasodilatation takes place whenever the organism has become accustomed to severe and 
excessive fluctuations of temperature. That this is true, experimental observations 
attests, whilst the unexposed portions of the body, such as the mesentery or internal org s, 
manifest none of the above reactive phenomena. 


We know that the face and hands become pale as the direct effect of 
cold, but subsequently flush if the individual is accustomed to cold and is in 
good health. In chronic disease, and in anaemic people, the reactionary 
reddening may not take place. The nude body, when exposed to cold and 
wind, may remain pale, with the surface vessels contracted whilst the skin 
of the face that is used to exposure, may react with a marked flushing. These 
well known phenomena of reactive hyperemia following cold are of importance. 
They should be borne in mind in prophylaxis. For, when the reactive 
dilatation is adequate, even severe degrees of cold fail to bring about gangrene. 
The factors that constitute the closing links in the chain of deleterious 
moments, and to which the gangrenous outcome is greatly due, may be 
summed up as follows. 

Firstly there may be an inadequate adaptation of the vascular system. 
Since the reaction of the vessels is intensified and prolonged through exer¬ 
cise, and climatic experiences, an absence of the latter would conduce to 
inadequate or insufficiently long dilatation, and subsequent vasoconstriction. 
In such circumstances the influence of cold, would bring about total plasmic 
changes and necroses, both by virtue of the action of the cold itself, as wed as 
through the insufficient oxygenation and nutritive supply. This explains 
the observation that soldiers are better able to withstand the cold and wet 
during the winter or early spring, than in the fall. 

Secondly, disease and weakness may cause the absence of insufficient 
reaction. Such individuals are unable to deliver as much blood and as many 
calories as are necessary for the conservation of any particular portion of the 
body when threatened. Gangrene due to freezing also was noticed more often 
when the extremities had been injured by bullet wounds, than when intact. 

Thirdly, tight body coverings, shoes, stockinettes, stockings, etc., may 
cause ischemia and constriction of the vessels by interfering with adequate 
reactive vascular dilatation. There must be enough room to accommodate 
the increased volume incident upon the dilatation of the vessels. 

The Effect of Stasis .—When the action of cold is prolonged and does not 
directly lead to freezing, the dilatation of the vessels loses its reactive nature. 
Whilst, it is ordinarily superseded by vasoconstriction, it would under such 
circumstances induce marked congestive dilatation of the capillaries. 

The flow of blood would become slower until the circulation finally 
ceases. The skin then takes on a bluish red or crimson red discoloration and 
edema of the tissues follows. Then blebs form. There is loss of the active 
muscular power, and loss of sensibility. In such a case, tissue death sets in 
and, after a time, macroscopic evidences of gangrene in the dry or in putrid 
wet stages, make their appearance. The important observations in this 


1 Sartorius, Inaug. Diss., Bonn, 1864. 


THERMIC GANGRENE 


179 


respect are those which have demonstrated that with a certain degree of tissue 
injury, the blood flow ceases in the dilated capillaries, although the afferent 
and efferent paths are open. Coagulation does not appear to occur at first, 
which is in keeping with the fact that occasionally the circulation can be 
again restored. This so-called stasis with interruption of circulation has not 
been altogether explained mechanically. This much, however, may be said, 
that when the tissue injury or insult has attained a certain degree, the blood 
ceases to circulate through the affected territory. This applies not only for 
the chemical or caustic injuries, but also for refrigeration. In the case of 
congelation it is probable that the tissue degeneration is the most important 
effect of freezing, whilst the circulatory disturbances and the stasis are accom¬ 
panying and secondary. When stasis occurs, tissue death is predestined. 

The Importance of Vessel Palsy .—A number of authors have attributed 
death of the tissues from cold to paralysis of the blood vessels. Wieting 1 
thinks that the essential factor in cases of protracted action of cold is the 
paralysis of the vessels which is occasioned by injury to the vascular inner¬ 
vation, and is followed by stasis and thrombosis. For this reason he speaks 
of the necroses occurring during the Balkan War as paralytic vessel gangrene, 
(neuroparalytic) gangrene of the vascular paralytic type (Marchand). 2 
Reference will be made on pp. 571 and 578 to the history of previous effects 
of cold in some of the cases observed. 

Both endarteritis and thrombosis have been considered as the causal 
factors, when the action of cold precedes the mortifying process by weeks or 
months. Indeed, it is assumed that the vessel endothelium is exceedingly 
susceptible to the action of cold. 

A number of authors in experimenting with the action of ether spray on vessels found 
that degeneration of the media and consequent proliferation of the intima with narrowing of 
the lumen took place. 3 It is interesting to note not only the immediate degenerative 
phenomena but the late proliferative condition of the endothelium. This suggests that the 
lesion is a replacement phenomenon, with substitution for the cells that had been destroyed 
(cicatricial in nature). The consequent narrowing of the lumina of the arteries is held 
responsible by some for the late gangrene. The eventual mortification is said to occur 
either by reason of the gradual impairment of circulation, or may ensue in such poorly 
nourished territories, whenever a secondary insult still further jeopardizes the circulation. 

Thrombosis .—Thrombosis is regarded as a rare cause of gangrene after 
freezing. Observation of experimenters along these lines, however, has 
shown that arteries dissected free and exposed to the strongest and severest 
degrees of cooling contained fluid blood so long as the vasoconstriction was 
insufficient to well nigh obliterate the lumen. Uschinski 4 could demonstrate 
thrombi only in some of the veins. 

There are three cases found in the literature in which extensive throm¬ 
bosis occurred after freezing. One of these was reported by von 
Recklinghausen 5 in a woman whose feet were frozen, and in whom the veins 
leading to the gangrenous toes were found thrombosed. Von Winiwarter 6 
described a case of widely distributed arterial thrombosis in a man who had 
been exposed to cold. Nagelsbach 7 described a case in which all of the large 
arteries of the foot and leg were thrombosed after freezing. It would appear 

1 Wieting, Zentralbl. f. Chir. ; 1913, p. 593, p. 1985. 

2 Marchand, Handb. d. allg. Path., 1908, Bd. 1. 

3 Zoege v. Manteuffel, Zentralbl. f. Chir., 1902, 3. 

4 Uschinski, Ziegler’s Beitr., 1893, p. 115. 

5 Recklinghausen, Deutsch. Chir. Lief. 2 and 3. 

6 Von Winiwarter, Langb. Arch., 1879, Bd. 23, p. 202. 

7 Nagelsbach, Munchen. med. Wchnschr., 1919, p. 353. 


180 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

therefore that although thrombosis may occur after freezing, it is a rather 
rare cause of gangrene. 

Prognosis—Opinions vary as to the criteria according to which a prog¬ 
nosis of the viability of a part subjected to cold is to be based. A persis¬ 
tence of pallor, coldness, lividity and anesthesia, has been regarded as of 
valuable prognostic significance. Certain authors (Meyer and Kohlschiitter ) 
believe that if spots of cyanosis, lividity and areas of anesthesia are present 
after a week, the affected part cannot be expected to recover. Other authors 
suggest the making of minute incisions in order to determine whether well 
oxygenated blood trickles forth from the wound. It has been suggested to 
apply the Moskowicz test. This in our opinion, would be contraindicated 
because of the danger of inducing thrombosis and vessel injury. . 

Therapy of Local Freezing.—Calcium salts, (particularly calcium lactate) 
because of their influence on the phagocytic power of the leukocytes and their 
stimulation of connective tissue formation, have been suggested as a means 




of combating the effects of freezing. In freezing of the third degree, it has 
been traditionally accepted that the thawing or warming should take place 
as slowly as possible. This does not pertain merely to cases of actual freez¬ 
ing, but also where the reduction of temperature has been less intensive. 
Cases of extensive gangrene are reported, and the occurrence of this compli¬ 
cation is attributed to sudden change of temperature. Some authors suggest 
rubbing with snow, others, such as Bundschuh, 2 employ cold water for 
almost an hour until the bath reaches the body temperature. If the frozen 
part regains its sensation and becomes red, minor lesions of the tissues 
may be prognosticated. When anesthesia and pallor persist, massage is 
recommended. Other authors recommend massage over long periods of 
time, continuing over twenty-four hours in half hour intervals. Kroh* is 
said to have revived extremities that presented all signs of impending 
gangrene. 

Other authors use the hyperemia treatment with or without baking. Ele¬ 
vation of the affected extremity is advised by Sonnenburg and Tschmarke. 4 

1 Meyer and Kohlschiitter, Deutsch. Ztschr. f. Chir., March, 1914, 127. 

2 Bundschuh, Miinchen. med. Wchnschr., 1915, No. 12. 

3 Kroh, Cit. by Florcken, Ergeb. d. Chir. u. Orthop., 1920, Bd. 12, p. 202. 

4 Sonnenburg and Tschmarke, Die Verbrennung u. d. Erfrierung, Ferd. Enke, Stuttgart, 
I9IS- 





GANGRENE DUE TO CHEMICALS AND DRUGS 


181 


Multiple incisions are regarded as of great value where the return venous 
circulation is impeded and are said to have been the determining factor in the 
saving of many limbs threatened by gangrene (Noesske, 1 Wieting 2 ). 

When the greater portion of the peripheral phalanges, is frozen, 
Bundschuh makes multiple incisions over the ventral and dorsal aspects of 
the phalanges. The schematic drawing (see Fig. 44) shows the situation of 
such incisions. The hyperemic treatment with elevation has been combined 
with this method. Other authors recommend the use of quartz light sub¬ 
sequent to the making of the incisions. Alternating hot and cold baths have 
also been suggested. 

It has been recommended by various writers that an effort should be made 
to convert moist gangrene into dry gangrene, and to this end the removal 
of the detached epidermis (Strohmeyer) has been advised. The application 
of dry dressings and powders, such as dermatol, finely pulverized charcoal 
and similar preparations, with or without the use of dry heat is frequently 
followed by good results. Even X-ray treatment (Wachtel 3 ) is said to 
have been of service. 

Operative Treatment/ —Conservatism is the watchword, and should be 
followed wherever possible. One should not be too hasty in pronouncing 
judgment regarding the eventual outcome, and operation should be deferred 
when one is in doubt. Early amputation is only then indicated, when com¬ 
plicating infection with phlegmon formation is imminent; or, when the septic 
resorption from a typical gangrenous territory serves as indication. 

Whilst the larger number of surgeons urge conservative therapy wherever 
possible, waiting for a line of demarcation to form and for sequestration to 
take place spontaneously, others lay great stress upon the advisability of 
obtaining a valuable functional stump. The latter proceed shortly after 
demarcation has become established, to the surgical measures that will 
assure such an issue. 


CHAPTER XXXII 

GANGRENE DUE TO CHEMICALS AND DRUGS 

Certain chemicals or drugs taken internally and applied locally may 
cause gangrene. Ergot, although not taken in the form of a drug, may be 
considered here as one of those substances that may produce gangrene 
when taken internally. Mercury, orthoform, phosphorus, carbolic acid, 
trichloracetic acid, strong acids and alkalies, may produce gangrene under 
certain conditions. 

The action of chemicals on cells and tissues is of manifold variety. They 
may combine with the proteids of the protoplasm and form more solid com¬ 
binations; or effect coagulation, dissolution and precipitation; or alter 
especially the colloids; or have an affinity for certain tissue constituents 
causing solution of lipoids and thereby destroying the construction of the 
cells. Poisons do not act like nutritive substances in proportion to their 

1 Noesske, Chir. Kong., 1920, Stuttgart. 

2 Wieting, Zentralbl. f. Chir., 1913 Nos. 16 and 52. 

3 Wachtel, Wien. klin. Wchnschr., 1917, No. 18. 


182 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


caloric value. They resemble rather the catalytic ferments in that they 
become the exciting factor in the mutation of normal stresses or forces, or 
exert a sort of restraining (paralytic) action on the normal processes. There 
does not seem to be any relation between poisonous activity and atomic 
weight, but rather some conformity with their valency. Varying effects may 
follow the application of one and the same substance according to its concen¬ 
tration; namely, stimulant, or paralyzing in weak solutions, inflammatory or 
suppurative in stronger concentration, or even with capacity for causing 
necrosis or gangrene. 

The source of these poisons may be the mineral, plant or animal kingdom. 
To these may be added those produced by pathogenic and saprophytic 
organisms, and those synthetically made up. Examples are arsenic, lead, 
mercury, and barium; of alkaloids, glycosides, proteins, toxalbuminates, 
enzymes, bacteria, and alien (heterologous) blood, (such as causes hemo¬ 
lysis, agglutination or precipitation). 

Substances that irritate the tissues severely may produce inflammation, 
suppuration or necrosis. Such are acids, alkalies, alkaline salts, metals, 
nitrogenous bodies and the irritating combinations of organic compounds. 
All acids have varying degrees of caustic action locally, according to the 
quantity applied and the concentration. When the cells, are killed off, 
direct necrosis, gangrene or mortification ensues. Even weak solutions (about 
5 per cent of muriatic, nitric or sulphuric acid, and caustic potash),may 
produce gangrene when applied as moist compresses for 20 to 24 hours. 
These drugs lead to maceration of the epidermis, necrosis, the deeper tissues 
becoming subsequently affected. Trichloracetic acid is also dangerous, if 
it be incorrectly used in the form of a wet dressing, when applied to remove 
surface warts. 

Sulphuric acid causes coagulation of albuminous substances of the tissues 
through withdrawal of water and heat production. The black eschars 
occasioned by it, however, are not expressions of carbonization, but due to 
the presence of derivants of blood pigment, such as hematin, acid methe- 
moglobin and hematoporphyrin. 

Nitric acid (over 33 per cent solution) causes immediate brownish-yellow 
discoloration. Proteids are precipitated by nitrification and changed into 
xanthoproteinic acid. There occurs coagulation of the blood in the vessels 
of the territory affected. 

Chromic acid also precipitates in its local action, its salts causing oxi¬ 
dation of cells. A greenish discoloration may result. 

Oxalic acid is caustic and dissolves collagenous tissues. 

Formalin or formaldehyde roughens the skin, hardens it, and brings about 
coagulation of albumin, having caustic and necrosing action on mucous 
membrane when sufficiently concentrated. 

In short, the acid group are caustics that may effect rapid disorganization 
of the protoplasm. This eventuality may be the result of withdrawal of 
water (suphuric acid), albuminous precipitation (organic and inorganic salts, 
fatty acids, trichloracetic acid), or through salt combinations with proteids 
(acid albumins). 

The halogens destroy the protoplasmic structure, in that they take up 
water and thus make salts that precipitate proteids. Chlorine and fluorine 
have the strongest action. Hydrochloric acid may lead to ischemic necrosis 
of the skin. So also chromic acid combinations may produce necrosis. 

The alkalies are not unlike the acids in their effects. However, these are 
characterized by the development of soft, smeary shreds of swollen disin- 


GANGRENE DUE TO CHEMICALS AND DRUGS 


183 


tegrated tissue—a true example of their dissolving effect (also called colli- 
quation or colliquation necrosis). 

Arsenic may have a caustic action in its oxidizing powers. 

Phosphorous is especially dangerous for its peculiar necrotizing effect on the 
jawbone, and there may even occur involvement of the vomer and sphenoid. 
These are the sequences of the inhalation of phosphorous fumes in the manu¬ 
facture of matches. Of the mercurial poisons calomel is a weak bichloride 
(sublimate) of mercury, an intensive caustic. The oxide, chloride and 
iodides combine locally at the site of application with the proteids, causing 
death and destruction of the cells. Mercury is reported to produce local 
sloughing at the site of injection, gangrenous patches in the gastro-intestinal 
tract, and sloughing of the skin. 

Silver nitrate combines with the proteids of the tissues to form a silver 
albuminate, appearing as whitish eschars that become dark through the 
action of light. In the blood this salt exerts a specific action on nerve cells, 
causing spinal paralyses, temporary paresis, paralysis of the vasomotor cen¬ 
ters and of the respiratory center. 

Although caustic effects have been noted in the stomach from the contact 
of lead, this poison is of no special significance as a clinical factor in the pro¬ 
duction of necrosis. The same may be said of zinc and copper. 

Local necrosis has resulted from the subcutaneous injection of the poison 
of bees and wasps . Serpent venom , too, has produced gangrene (in case of the 
crotalidae). 

Finally, we may mention the distinctive effects of some of the microbic 
poisons. Tuberculin (old) and mallein in concentrated form may bring about 
necrosis. Substances of similar action have been derived from the bacillus 
pyocyaneus, prodigiosus, proteus and penicillium glaucum. Cell necrosis, 
too, may follow the action of ectotoxins. 

The bodies of bacteria endotoxins have similar effects. 

A gangrenous form of eruption is recorded in the literature as following 
the use of orthoform. Gangrenous patches and ulcerations are said to com¬ 
plicate the use of this drug about the fingers, anus and nipples. 

Carbolic Acid Gangrene— The fingers or toes are usually affected follow¬ 
ing the local application of ointments or wet dressings. The gangrene may 
result after the application of even a very weak solution (such as 0.5, 1 or 2 
per cent). After the dressing has been applied for a few hours, the finger or 
part becomes blanched, and a pricking sensation is felt. Within 24 hours 
or less, the skin becomes dusky, discolored, dry gangrene may occur, the part 
becoming gradually mummified. 

Various theories have been offered to explain the cause of gangrene from 
the use of weak solutions of carbolic acid. According to one view, thrombosis 
is produced in the peripheral vessels; according to another, a particular 
action upon the trophic functions and vascular nerves is exerted. 

Amputation is advisable according to the view of Leclerc 1 who bases his 
conclusion on the following observation. 

A woman 50 years old, despite the fact that she was given accurate proportions for a 
phenol dressing, to be applied to the finger, applied a compress saturated with the pure 
solution for 24 hours without any sensation of pain. Upon removal of the dressing the 
finger was found dead white, shriveled, and at the end of 6 days it became gangrenous. 
Two days later pain of the hand was experienced and “erythema’/ on the back of the hand 
developed. Symptoms of disturbed mentality now followed, with extension of the gan¬ 
grene, and the following day elevation of temperature (38° in the morning and 38.3 in t e 
evening) and pulse 140. Then came a state of collapse and exitus on the following day. 

1 Leclerc, Bull, de l’Acad. de med., Paris, Feb. 25, 1919, 81, 205. 


184 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Lysol , too, may be regarded as dangerous in solutions that are not 
thoroughly mixed, as the case of Sowles 1 demonstrated. 

In a patient who soaked his right index finger over a total period of about 15 minutes in 
a basin of water, into which an “indefinite amount” of lysol had been admixed, the distal 
half of the finger became intensely swollen the following day. Examination, 24 hours later, 
demonstrated marked redness and swelling with a sharp line of demarcation. The epider¬ 
mis of the dorsal distal half of the finger was white and raised from the subcutaneous tissue, 
appearing to be dislodged by serum or pus. However, on removal of the dead skin, the 
subcutaneous tissues were evidently dry and gangrenous. 

In the following case observed by von Stapelmohr 2 the agent was a 5 per 
cent solution of lysol. 

A woman of 53 had cut her left thumb 4 days before coming to the clinic. Two days 
after the accident she had wrapped her thumb in a lysol drenched bandage for 12 hours, 
and later had held the thumb for 2 hours in the same 5 per cent lysol solution. 

Upon examination the skin was slightly red with occasional small blisters. In the next 
few days the terminal phalanx became black, and n days after the injury the finger 
was amputated, at which time the soft parts were also attacked by dry gangrene. 

Gangrene Due to Poisonous Gases.—Thrombosis in both deep and 
superficial vessels (veins) may succeed the inhalation of a number of differ¬ 
ent toxic fumes and gases. As examples of such we may quote some of 
the records of gangrene due to carbon monoxid and illuminating gas. After 
exposure to carbon monoxid from a charcoal stove, the following condition 
is reported as having resulted in one case (Thandavaroyan 3 ). 

Areas of hyeremia were observed confined entirely to the left side of the face, left hand, 
lower part of the chest and left thigh. Although the hyperemic areas on the face and chest 
disappeared after a few days, raised anesthetic areas appeared on the left hand and thigh. 
Four days later gangrene of the little finger of the left hand set in, with absence of circula¬ 
tion in the other fingers of that hand. The dry gangrene was well demarcated; the swelling 
of the hand and thigh improved under treatment; amputation was refused. 

Briggs 4 * relates this instance. 

After accidental disconnection of a pipe line on a motor boat unbeknown to the patient, 
he retired to his cabin, where he was soon after found unconscious. 

Upon examination it. was found that the backs of both hands and feet were covered with 
large tense blebs. In spite of conservative treatment, extensive gangrene of both upper and 
lower extremities rapidly developed, and on January 24, 1919 his condition was as follows. 

Right hand—gangrene of the entire three middle fingers, inner border of the thumb and 
little finger. 

Left hand—gangrene of the distal phalanges of the four fingers and flexor surface of the 
thumb. 

Right leg—gangrene over outer border of tibial region, external malleolus, outer border 
of dorsum of foot and small patches on three toes. 

Left foot—gangrene of two toes. 

The necrosis attacked the skin, muscle tissue, tendon, periosteum and bone, as also 
several joints. 

January 28, 1919 (37 days after the accident) amputation of the following members was 
performed. Right-hand—disarticulation of 3 fingers; left hand—4 fingers. 

Riedel 6 reports a case of gangrene of the leg after illuminating gas poisoning. 

Several days after an attempted suicide with illuminating gas a woman was attacked by 
nausea, abdominal pains and stiffness of both legs attended with pain in the legs. After 
7 days the posterior tibial and anterior tibial arteries became thrombosed (probably as the 
result of the prolonged retention of carbon monoxid in the blood). 

1 Sowles, Boston Med. & Surg. Jour., 1919, p. 510. 

2 von Stapelmohr, Hygeia, 1917, 79, 438. 

3 Thandavaroyan, Lancet, April 30, 1921, 1, 910. 

4 Briggs, Jour. Am. Med. Assn., Aug. 30, 1910, 73, 678. 

6 Riedel, Deutsch. med. Wchnschr., June 9, 1921, 47, 651. 


GANGRENE DUE TO CHEMICALS AND DRUGS 


185 


Gangrene Following the Injection of Medicaments.— A few examples of 
gangrene following hypodermatic or subcutaneous injection of adrenalin, 
arsphenamin, quinine, and after simple hypodermoclysis, may suffice to 
illustrate. 

Following injection of glucose solution with adrenalin , Guilera 1 reports a 
case. 

A primipara of 23 years after receiving 2 injections of 350 grams of glucose solution with 
adrenalin into the right thigh developed a gangrenous area. The necrosed zones were 
extirpated and the dead tissue removed “en bloc” down to the aponeurosis. 

In this case the gangrene was not due to the volume of the liquid injected 
nor to any defect in preparation of the solution, or in the technic of the injec¬ 
tion. . The writer attributes it to the vasoconstrictive action of the adrenalin 
contained in the glucose serum in an anemic, infected person. 

Muller 2 reports gangrene after subcutaneous injection of sodium chlorid. 

Because of post-partum hemorrhage in a female 29 years of age, 1000 cc. sodium chlorid 
solution were injected subcutaneously into the thigh. Two days later about 20 cm. from 
the site of injection the skin of both thighs became dark blue and blistered. Gangrene 
spread rapidly. The patient left the clinic unrelieved. 

. In explanation of the gangrene the author believes a chemical effect could be ruled out 
inasmuch as the solution was made up correctly; that a thermal injury was not responsible, 
inasmuch as the temperature was controlled, and was in reality too cold (35°); that no 
bacteria which might cause the infection were found at 37.4 0 ; and further, that injection 
into the fascia (which Jungmann believes to be an important cause of gangrene following 
sodium chlorid injection) did not occur in this case. The only remaining etiological factor 
could have been the pressure necrosis such as is described by Liepmann. This is caused by 
delayed resorption and consequent prolonged pressure effect upon the surrounding tissue 
and capillaries. 

Gangrene Following Injection of Quinin— According to Prat, Flottes and 
Violle 3 quinine necrosis is exemplified by the following report. The patient 
received about 10 aseptic injections of chlorhydrate of quinine into the 
gluteal region, and after about 2 weeks a small focus of induration was 
observed. Three to 4 days later the region began to swell, the skin became 
stretched without reddening, and sensitive to pressure, soon resulting in a 
deep mass. 

If an incision be made in such a case at this period, necrotic tissue is 
exposed. The quinine determines an amicrobic mortification, an aseptic 
necrosis of the tissues. The cellular tissue is the most altered, the skin in¬ 
tact. The muscles are changed later; groups of fascia become indurated and 
mortified; veritable blocks of necrosed fibers are easily detached from the 
healthy muscle fascia. Finally the cellular tissue is filled with pus and the skin 
drops off in gangrenous shreds. 

Left to itself, quinine necrosis would end in sphaceli, extensive detach¬ 
ment and bacterial suppuration. In the “quinine abscess” globules of pus, 
degenerated leukocytes, pyogenic microbes, blood corpuscles and fatty 
granulations are observed. The formidable decay of quinine necrosis gener¬ 
ally necessitates surgical intervention under chloroform anesthesia. This 
consists in wide and deep incisions, going beyond the limits of the affection 
and excision of the mortified tissues. 

Sutter 4 records gangrene of the fingers due to the injection of arsphenamin. 

1 Guilera, Rev. espan. de med. y drug., Barcelona, 1919, 2, 664. 

2 Muller, Med. Klin., Aug. 1, 1920, 16, 804. 

3 Prat, Flottes and Violle, Bull, de l’Acad. de Paris, April 10, 1917, 77, 506. 

4 Sutter, Jour. Am. Med. Assn., Nov. 22, 1919, 73, 1611. 


186 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In case O. P. M., aged 35, immediately after the injection of 0.4 arsphenamin diluted 
in 250 cc. of normal salt solution, into a vein of the left arm, there was severe pain in the 
hand and the peripheral circulation was poor. According to the history there was evidently 
some infiltration about the site of the intravenous injection. Subsequently dry gangrene 
of the distal portion of all the fingers took place, the index finger being involved up to the 
middle phalanx, and the middle finger to a somewhat less degree, the ring finger up to the 
middle of the second phalanx. Amputation of the thumb distal to the first phalanx, 
of the index finger 1 cm. proximal to the middle phalangeal joint, disarticulation at the 
middle phalangeal joint of the middle finger, and of the middle phalangeal joint of the ring 
finger were carried out approximately 3 months after the injection of arsphenamin. 

Gangrene Due to Ergot. —This results from eating bread made of spurred 
rye, and has not been observed when ergot is taken for medicinal purposes. 
This disease was not uncommon in the eighteenth and early part of the nine¬ 
teenth centuries, particularly in Europe, where epidemics of so-called ergotism 
are known to have occurred. At present it occurs but rarely, and then only 
sporadically. Two types are described, a convulsive and a gangrenous type, 
although both types may be combined. 

After prodromal gastro-intestinal disturbances, such as diarrhea, colic, 
occasional vomiting, disturbances of the circulatory and nervous systems 
appear. The extremities may become cold, numb, blue; the pulses may 
become weak and muscular spasms may occur. When the spasms become more 
general, seizures of an epileptic nature develop. In the gangrenous type of 
case, either the toes or fingers are usually affected. They become cold pain¬ 
ful, show cyanotic or purplish patches which gradually mortify, gangrene 
being usually of the dry type. 

Cases described as occurring in southern Russia are said to begin with 
formication, coldness, numbness of the fingers and toes, gradually resulting in 
bluish black discoloration, drying and detachment of nails with necrosis of 
parts or whole fingers or toes. Either dry or moist gangrene may affect the 
peripheral parts, including even the nose and the ears, and may be accom¬ 
panied by severe pain that disappears with sequestration of the tissues. In 
the mild cases small islets of epidermis only are separated, or blebs appear and 
the hairs fall out. The gangrenous blebs are analogous to those of herpes 
zoster gangrenosa. 

At other times the malady may remain latent until an intercurrent disease 
such as pneumonia, scarlet, typhoid, and so forth activates it. Then severe 
lesions, such as gangrene of the lung, skin, intestines and of the female sexual 
organs, may develop. 

The three chief actions of ergot, namely, its spastic influence, uterine 
stimulation and production of gangrene have been referred to three different 
toxic elements; the first, to ergotin and ergo toxin; the second to p hydro- 
xyphenylacthylamin; and the third to sphacelinic acid and to sphaceotoxin 
(Robert’s appellation, sphacelinic acid so derived from the Greek word 
sphakelos meaning gangrene). Other authors, however, ascribe this action 
to an amorphous alkaloid “ergotoxin. ” The preparation of Robert 1 2 3 is effec¬ 
tive on the peripheral parts, when diluted solutions are taken internally; 
while in concentrated form it causes necrosis at the site of application— 
pharynx, and gastro-intestinal canal. Even fowl (especially the cock) 
when fed with ergot show symptoms, and the tips of the cock’s comb are 
reported as showing necrosis as well as the tongue and wings. 2,3 Von 

1 Robert, Arch. f. exper. Path., XVIII, 1884; also Lehrbuch der Intoxikationen, Stutt¬ 
gart,! 906. 

2 Griinfeld, Arb. d. pharmak. Inst. z. Dorpat, XI, 1890; VIII, 1892; XII, 1895. 

3 Jacoby, Arch. f. exper. Path., XXXIX, 1897. 


MICROBIC GANGRENE 


187 


Recklinghausen found hyaline thrombi in the arterioles, and hyaline degener¬ 
ation of the vessel walls in the affected regions of these experimental animals. 

In explanation of the physiologic action of the poison on the vessels von 
Recklinghausen offers certain conclusions deducible from his pathologic 
findings. Noting a ring-like zone of red blood cells between the hyaline vessel 
wall and the hyaline thrombus, this author concludes that a primary vessel 
contraction, attended with stasis and hyaline thrombosis of the contents, is 
followed by relaxation, dilatation of the vessel allowing a renewed current to 
be established between clot and vessel wall. According to this theory, the 
necrosis would be due to the vascular disturbances, and gangrene of this type 
should more correctly be grouped under the vascular forms. Such a theory 
would find confirmation in the similarity of the poison’s action on the uterine 
and vascular musculature, on both of which a contractile effect is produced. 


CHAPTER XXXIII 

MICROBIC GANGRENE 

The more important types of microbic gangrene are (i) hospital gangrene , 
(2) noma , (3) emphysematous gangrene , and (4) gangrene due to virulent pyo¬ 
genic organisms (. streptococci , etc.). 

1. Hospital gangrene (sloughing phagedena, pulpy gangrene, putrid degen¬ 
eration, traumatic typhus, nosocomial gangrene) has practically disappeared 
since modern antiseptic methods have been introduced into surgery, and need, 
therefore, but slight mention here. It occurred either in epidemics, or was 
endemic in hospitals, particularly in the military hospitals. Hospital gan¬ 
grene may be regarded as an acute progressive gangrene with putrid decom¬ 
position or degeneration of the wound, initiated by local symptoms, but 
followed rapidly by severe constitutional manifestations. The cause is doubt¬ 
less an infectious one, anaerobic bacilli being probably responsible. Mat- 
zenauer claims to have isolated a bacillus 1 which however, he could not 
demonstrate in pure culture. Nasse 2 found an ameba. 

According to the clinical course, authors have described a superficial and 
a deep form, and according to the external manifestation an ulcerative and a 
pulpy variety. 

Erichsen 3 describes the disease as follows. “ A disease characterized by a 
rapidly destructive and spreading ulcer, covering itself as it extends by an 
adherent slough, and attacking open sores and wounds. When sloughing 
phagedena invades a wound that is previously perfectly healthy, the surface of 
the sore becomes covered with gray, soft points of slough, which rapidly extend 
until the whole of the ulcer is affected. At the same time it increases rapidly in 
superficial extent, and commonly in depth; the surrounding integument 
becomes edematous, swollen, and of a vivid red color; the edges of the ulcer 
are everted, sharp-cut, and assume a circular outline, and its surface is covered 
with a thick, pulpy, grayish green, tenacious mass, which is so firmly adherent 
to the sore, that it cannot be wiped off from it, being merely swayed to and 

1 Arch. f. Dermat. u. Syph., Bd. 55. 

2 Arb. aus von Bergmann’s Klinik, 5ter Teil, 1891. 

3 Science and Arts of Surgery. 


188 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

fro when an attempt is made to clean it. There is usually some dirty, yellow¬ 
ish green or brownish discharge, and occasionally some bleeding, the pain is 
of a severe burning, stinging, and lancinating character, and the fetor from the 
surface, is considerable. The ravages of the disease when fully developed are 
extensive. The soft parts, such as the muscles, cellular tissue, and vessels, 
are transformed into a gray, pulpy mass and the bones are denuded and 

necrosed.” 1 . . 

The diphtheritic form is characterized by certain alterations in previously 
healthy, granulating wounds. Associated with fever and pain, there appear 
yellowish-brown areas of discoloration in the granulation, hemorrhages and 
superficial sloughs. The diphtheritic form may become ulcerative when dis¬ 
integration of the surface takes place. The discolored areas will soon give 
rise to a foul odor, leave sharply demarcated ulcers which rapidly fuse together, 
or the bottoms of the ulcers become hemorrhagic and gangrenous, their mar- 
gins eroded, the neighborhood, tender and painful, and inflamed far beyond 
the zone of the wound. 

The Pulpy Form— Marked swelling takes place here, gas may develop 
in the tissues, a mass or pulp being developed, which may be likened to brain 
substance. Associated with it, extensive hemorrhages may give rise to the 
hemorrhagic type. In the superficial form the process would often be self¬ 
limited, whereas in the deep form a putrid phlegmon would develop, leading 
to bone necrosis, even ulceration of vessels, and death due to hemorrhage. 
Or, the deep form may be associated with toxic general symptoms, that lead 
to a lethal outcome within two or three days. 

As complications, erysipelas, metastatic foci of pus, and lymphangitis 
have been described. 

Treatment— This consists of the rapid and energetic cauterization of 
putrid areas with Pacquelin cautery, opening of the abscesses and surgical 
cleanliness. Sloughs are to be removed, and general stimulants freely 
administered. 

2. Noma.—This form of gangrene, also called cancrum oris , gangrenous 
stomatitis , cancer aquaticus , is a special form of ulcerative stomatitis with 
gangrene, that occurs almost exclusively in children between the ages of two 
and twelve, and often follows some debilitating disease. The affection has 
its origin in an infiltration of the mucous membrane in the neighborhood of 
the angle of the mouth. The exudate or infiltration then becomes gangre¬ 
nous, and converted into a bluish-black, dry mass, which is cast off, the morti¬ 
fying process progressing, however, in the depth and laterally, so as to involve 
the lips, chin and cheeks. Within a few days a considerable portion of the 
cheeks becomes destroyed and even the bone becomes exposed and necrotic. 
Rather characteristic is the perforation of a cheek which may ensue within a 
few days. Externally, in the pale, swollen cheeks, a bluish-black hard spot 
with a reddish zone of demarcation appears, or with this, there may be 
associated a large bleb. After the gangrenous area is cast off, the perfora¬ 
tion or hole is left leading into the cavity of the mouth (Fig. 45). 

The disease seems to affect poorly nourished children, often in the course 
of an infectious disease, such as measles, scarlet or typhoid. As a rule, 
fever, cerebral symptoms of loss of consciousness accompany the malady 
which is fatal within two or three weeks. 

The etiology does not seem to be the same in all cases. Schimmelbusch 1 
and Babes 2 isolated a special type of bacillus. Perthes found a streptothrix. 

1 Deut. med. Wchnschr., 1889. 

2 La Romaine Med., 1894. 


MICROBIC GANGRENE 


189 


Others, such as Buday 1 believe that a spirillum and a fusiform bacillus growing 
in symbiosis are responsible for the affection. 

Rods and spindel shaped elements were found by Perthes 2 and regarded as variant 
developmental forms of a strep to thrix (cladothrix of Seiffert). Baumgarten takes excep¬ 
tion to the theory of bacterial causation, believing the organism found to be secondary 
invaders. However, the finding of spirillae in the areas of advancing gangrene is believed 
to be suggestive of a bacterial influence. Bernheim and Popsischill 3 found fusiform bacilli 



Fig. 45.—Defect in cheek produced in noma. {Lexer.) 

and spirochetae, but in the depth a mere plump rod. This latter is regarded as the true 
exciting organism. Hoffmann and Kiister 4 also identified a bacillus as the causative agent. 

The peculiar sharp delimitation and separation of the pulpy putrid tissue has been inter¬ 
preted as indicating some nerve derangement. Latterly, however, the dominant view 
seems to be that noma is a form of putrid infection with gangrene as a prominent feature. 
Being frequently one of the complications of other diseases, measles, typhus, diphtheria, 
dysentery, mercurial stomatitis, syphilis, etc., it is still a mooted question as to whether 
it is a reactionary sequel of other infections, or of unique causation. 

In view of the varied results of bacterial studies, it is quite compre¬ 
hensible that noma cannot as yet be considered an entity as far as etiology 
is concerned. 

Treatment .—This consists in the destruction of the gangrenous areas with 
the Pacquelin cautery, frequent irrigations of the mouth, prevention of aspira¬ 
tion pneumonia, and, according to some authors, the extirpation of the 
affected area with the knife. As prophylactic measures, the mouths of all 
children suffering from severe debilitating illnesses should be kept scrupu- 
ously clean, all ulcers should be cauterized, and carious teeth carefully 
attended to. 

1 Beitr. z. path. Anat., 1905, XXXVIII. 

2 Perthes, Munchen. med. Wchnschr., 1902. 

3 Bernheim and Popsischill, Jahrb. f. Kinderh., 1898, XLVI. 

4 Hoffmann and Kiister, Munchen. med. Wchnschr., 1904, 43. 


190 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XXXIV 

MICROBIC GANGRENE (CONTINUED) 

GAS GANGRENE 

Emphysematous Gangrene (microhic or traumatic spreading gangrene , 
gangrene foudroyante ) produced by rapidly spreading infection of the sub¬ 
cutaneous tissues is a clinical symptom-complex produced by a number of 
different virulent gas-producing organisms. Much confusion has arisen 
regarding the nomenclature and etiology, authors, however, being generally 
agreed regarding the intensity of the infection, its virulence, the production 
of gangrene and the presence of gas in the tissues. It has been variously 
termed, traumatic emphysema, gas phlegmon, acute microbic gangrene, 
fulminating gangrene, gangrenous cellulitis, malignant edema, anaerobic 
gangrene. 

Numerous appellatives have been employed, most of which have merely 
historical interest. The French authors describe it as bronze erysipelas, a 
gangrene foudroyante. If the gas bacillus or the bacillus of malignant edema 
alone were responsible, the terms, malignant edema or malignant emphysema 
would be apt. However, numerous other organisms are known as causative 
agents. Gas edema as been suggested by Aschoff. Other names are gas 
inflammation and phlegmon, or gas gangrene. The last of these has found 
wide acceptance, even though the pathological process does not attain the 
state of tissue mortification, and is more correctly a gas phlegmon. The 
multiplicity of names is partly due to the diversity of the infecting organisms 
and the consequent variations in the objective phenomena. 

The Bacteriologic Etiology. —Although the gas bacillus (B. aerogenes 
capsulatus) of Welch (and Nuttall) or of Frankel and the bacillus of malig¬ 
nant edema were formerly regarded as the sole causative agents, more recent 
researches have shown that a number of other obligate anaerobic bacilli can 
be cultivated. The bacteria can be described in two groups; {A) the non- 
putrefactive, and ( B ) the putrefactive form. 

A. The Non-putrefactive Type.—i. The Welch or Frankel gas bacillus (bacillus 
phlegmones emphysematosce). 

Morphology. —The Welch or Frankel gas bacillus (described by French authors as 
Bac. perfringens) is found in the earth, dust, soiled uniforms of soldiers, trenches and in the 
intestines. It is a short plump bacillus with square end, immobile, without flagellae. It is 
absolutely Gram positive, and can be demonstrated to possess a capsule (Buerger method). 
Spores can be but rarely demonstrated. 

It is easily cultivated according to the usual anaerobic methods. It can be most easily 
recognized and cultivated by animal inoculation with the employment either of a rabbit in 
whose ear vein a culture is injected intravenously, or by subcutaneous injection into a 
guinea pig. In these animals, if they be killed shortly after inoculation, and placed into the 
incubator, intensive gas production can be demonstrated. 

Toxins and Antitoxin Formation.—The question as to the production of 
toxins is still a mooted one. Certain authors have found that sterilized 
cultures are not virulent for guinea pigs. Passini, however, claims to have 
found toxic substances in the cultures of gas bacilli that are lethal for the 
animal. Klose reports the isolation of a toxin in cultures, which produces 
hemorrhages and local necrosis in guinea pigs; and, when injected intraperi- 
toneally, causes dyspnoea, fever and death. Intravenous injecotin was 


MICROBIC GANGRENE 


191 


followed by spasm and rapid exitus, the liver and spleen showing hemorrhages 
and marked anemia. 

By the appropriate treatment of dogs and rabbits, this author was able 
to produce an antitoxin with which he could protect guinea pigs against a 
lethal dose of the organism. 

2. The Bacillus of Malignant Edema. 

Morphology.—Several types of bacillus of malignant edema have been described; a 
Gram negative type with flagellae, and highly pathogenic for rabbits and goats. These 
animals succumb in a very short time with severe symptoms of malignant edema. In stab, 
gelatin cultures, a cylindrical or bell-like fluid liquifaction takes place. 

A Gram positive type has been recognized. This is pathogenic for guinea pigs, the 
animals dying within 24 hrs. with marked edema. Rabbits, however, are non-sensitive to 
this type, except for slight local edema that rapidly disappears. 

A third type is also Gram positive, is also pathogenic for rabbits and guinea pigs and is 
said to be identical with Aschoff’s gas edema bacillus. 

Pfeiffer and Bessau 1 distinguish between the bacillus of malignant edema which is unable 
to produce putrefaction, and similar bacilli of the putrefactive type, and which can produce 
edema, although considerably less malignant than the true bacillus of malignant edema. 
The latter bacillus is longer and more slender than the Frankel-Welch bacillus, its ends more 
slender and may grow in long forms. It has motility by reason of numerous flagellae. It 
is variable to the Gram stain and frequently the majority of the bacilli are negative to Gram. 
The spores are oval, usually central, in no way causing bulging of the bacillus. 

In guinea pigs subcutaneous inoculation with the bacillus of malignant edema, a charac¬ 
teristic bloody exudate is produced without or with very slight gas production. Exitus 
takes place early, and the bacilli can be cultivated after death both locally and in the inter¬ 
nal organs and blood. Intravenous injection in rabbits is so toxic that death occurs within 
a period insufficient to warrant the expectation of multiplication of the bacilli. The toxic 
effect of the cultures seems adequate to cause death. 

Toxin Production.—Ficker 2 and Silberstein 3 were able to isolate toxins and the latter 
author by the elaboration of a goat serum could neutralize the effect of a lethal dose 
in guinea pigs. 

3. The Aschoff Gas Edema Bacillus. 

This author was able to isolate (1915-1916) a plump motile anaerobic bacillus appearing 
in diplobacillus or chain forms, usually Gram positive, but occasionally negative. Spores 
were noted in a central or terminal situation. In milk, gas formation and coagulation 
take place. It is distinguished from the Frankel-Welch bacillus through its motility. 
It differs from the Ghon-Sachs bacillus being more virulent for rabbits. 

B. Putrefactive Organisms. —1. Th ePfeiffer-Bessau bacillus. This organism has been 
called the watch-hand (Uhrzeigerbazillus), has constant characteristics, more probably 
identical with the bacillus putrificus (Bienstock). These are short Gram positive rods with 
rounded ends and marked motility. Their spore formation is active, so that most of the 
bacilli contain large mobile spores. These are usually terminal and cause an intumescence 
in the body of the bacillus. They are but slightly pathogenic. Subcutaneous injection in 
guinea pigs produces local inflammatory infiltration; intravenous injection into rabbits is 
harmless. 

2. The Pfeiffer-Bessau Par oedema Bacillus. —This organism has morphologic similarities 
with the bacillus of malignant edema, but differs from it in its putrefactive powers. This is 
not a single group, but its members show considerable variation. 

The paroedema bacillus varies in size resembling that of malignant edema, poorly 
motile or non-mo tile; some Gram positive, others Gram negative. The spores do not 
alter the width of the organism and are usually central. They are but slightly pathogenic. 
This type includes a group of organisms not absolutely similar. 

3. The von Hibler Bacillus. 4 —This is a motile rod and usually a diplobacillus. The 
spores are frequent and dilate the bacillus. It is Gram positive, but not as strongly as the 
Welch bacillus. It is pathogenic for guinea pigs, white mice, rats, rabbits, etc. Except 
for the observations of von Hibler, there are only those of Chiari regarding the occurrence 
of this in gas phlegmon of human beings. 

1 Pfeiffer and Bessau, Deutsch. med. Wchnschr., 1917, p. 1217, 1255, 1281. 

2 Ficker, Med. Klin., 1917, No. 45, 118. 

3 Silberstein, Wien. klin. Wchnschr., 1917, No. 52, 1672. 

4 von Hibler, Zentralbl. f. Bakteriol. Parasitenk. u. Infectionskr., 25, 513, 1899 also 
Untersuchungen u. d. path. Anaeroben, Fischer, Jena, 1908. 


192 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


4. The Ghon-Sachs Bacillus —This is a strong anaerobic pleo-polymorphous coccoid 
bacillary organism sometimes, shred-like, or fusiform. In some of the preparations 
bifurcations have been noticed. It is motile and has lateral flagellae. Spores may be 
central or terminal. The bacilli are Gram labile, the young forms Gram positive, the older 
ones but weakly so. There is no capsule. 

Guinea pigs are killed by 0.5 cc. of a 48 hr. sugar culture, death being preceded by gas 
formation, edema and hemorrhage. Intravenous injection into rabbits produces death 
with extensive edema. 

Toxins have been produced by Ghon and Sachs. The Welch experiment of intravenous 
injection into animals results positive for gas formation when the animal is kept in the 
incubator after death. 

Anaerobic Bacilli .—Organisms have been found in gas gangrene, whose causal relation¬ 
ship to the lesions has not been established. Of these, there are the Novy 1 2 bacillus and the 
Conradi-Bieling 3 bacillus. 

The former is an aerobic, motile Gram positive bacillus without spores, characterized by 
the presence of long and fixed forms, but slight motility, absence of spores, poor growth on 
agar and strong pathogenic action on experimental animals. 

The Conradi-Bieling bacillus resembles those described by Aschoff. The vegetative 
form is a non-motile, Gram positive thick rod, producing marked gas formation, in carbo¬ 
hydrate media, and liquefaction of proteid media, very pathogenic for guinea pigs that die 
of hemorrhagic edema and gas formation, whilst rabbits are non-sensitive. 

Relationship of the Various Bacteria. —The most dangerous of the bacilli that produce 
gas gangrene are the Frankel-Welch and the bacillus of malignant edema, neither being 
putrefactive types. 

The organism found in gas gangrene has been detected in the earth and in the intestinal 
tract. This explains their easy entry into wounds, particularly during war. The Frankel- 
Welch bacillus is the most common of the organisms found. 

Next in frequency is the bacillus of malignant edema as a causative agent in an aerobic 
wound infection. 

Clinical gas gangrene, it is true, is most frequently due to the Welch or edema bacillus, 
but anaerobic mixed infection is common. Thus, the tetanus bacillus is not infrequently 
admixed in such infections. 

Furthermore, anaerobic bacilli may be associated with aerobic organisms, namely, with 
streptococci, staphylococci, bacillus coli, bacillus pyocyaneus, proteus and others. The 
streptococcus is particularly important, indeed, may be so preponderating so as to appear 
to be the gas producing organism. 

Some authors believe that certain of the gas producing organisms may be changed into 
other types. Thus such mutation is said by Aschoff to occur, also by Conradi and Bieling, 
when a vegetative form of gas bacillus is without spores and flagellae and is grown upon 
proteid media. A conversion into a flagellated, spore-bearing form results. Other authors, 
such as Frankel, desire to controvert this assumption, suggesting that such observations 
were due to the presence of a mixed infection. 

Pathological Anatomy.—The most important lesions in gas gangrene 
are those occurring in the musculature, the alterations in the other tissues 
being secondary. The muscle becomes pale red, dry and filled with small, 
glittering, silver-like gas bubbles. Later, it takes on a brownish or blackish 
tone with greenish tint and the gas bubbles enlarge. Then fluidification of 
the muscle into a blackish, brown, pasty substance with large gas bubbles 
occurs. At a distance from the primary focus, the muscle undergoes areas of 
waxy necrosis, becomes greyish-yellow and like fish meat. Associated are 
small hemorrhages giving the muscles a variegated appearance. The inter¬ 
muscular connective and subcutaneous tissues are at first infiltrated with a 
brownish yellow edematous fluid, that is striking because of its large amount. 

Microscopic examination also reveals characteristic changes particularly 
in the muscle tissues. The gas bacilli are present in large numbers, accumu- 

1 Ghon-Sachs, Zentralbl. f. Bakteriol., 34, No. 4-7, 1903; also 35, No. 6, 1904; also 
36, No. 2, 1904. 

2 Novy, Ztschr. f. Hyg., 17, 1894. 

3 Conradi-Bieling, Feldarztl. Beil., Miinchen. med. Wchnschr., 1916, 133 (49), 1023 
(455), 1561 (705); also Berl. klin. Wchnschr., 1917, No. 19, 449. 


MICROBIC GANGRENE 


193 


lating in the connective tissue and fatty septa, extending to the subcutaneous 
tissue and diminishing in number towards the skin itself. In the lumina of 
the veins, occasional gas bacilli will be found, but not in the arteries. 

Microscopically, therefore, the situation of the bacilli corresponds to the 
assumption that the lesion is primarily one of the muscle. However, to be 
exact the bacilli actually lie first, in the perimuscular or perifascicular con¬ 
nective tissue and in the lymph spaces. By virtue of the activity of the bac¬ 
teria the muscle fibers undergo fluidification with gas formation, there being an 
absence of any inflammatory and cellular reaction. Rounded spaces about 
the muscle fibers represent the gas bubbles. Pari passu with gas formation 
there is a continuation of the degenerative condition of the muscle. The 
fibers of the latter become fragmented, degenerate into hyaline bodies and into 
minute particles. All of these detached and separated pieces of muscle 
element become fluidified into a structureless mass, in which no recognizable 
histological elements are then to be found. The absence of inflammatory 
reaction is characteristic for pure gas bacillus action, for leukocytic infiltra¬ 
tions usually indicate mixed infections with cocci. In addition, there is 
marked edema of all of the tissues. 

The three stages in the development of the destructive lesions are recog¬ 
nized by certain authors. 

First.—A primary focus develops characterized by the entrance of a foreign 
body (piece of clothing or shot) in a bullet tract; in it there is more or less gas 
formation in the subcutaneous tissue and musculature. In this zone there 
are numerous bacilli with spores and also free spores. 

Second.—Adjacent to this and varying in width there is a zone of strong 
hemolytic edema of the subcutaneous tissue with gas bubbles, containing 
bacilli without spores. 

Third.—A third zone without bacilli but with toxic yellow edematous fluid 
infiltrating the tissues. 

Gas Formation in the Internal Organs. —Welch and Nuttall 1 called atten¬ 
tion to gas formation in organs due to the action of the bacillus aerogenes 
capsulatus. Although the occurrence of gas formation in the organs was at 
first demonstrated postmortem in experimental animals, Welch believes 
that such gas formation can occur during life. Other authors take excep¬ 
tion to this view. 

The more recent observation during the war period would concede the 
possibility of antemortem changes of this nature, with, however, the reser¬ 
vation that such occurrence precede the lethal outcome by but a short time. 

The Blood Vessels. —In cases of gangrene due to infectious processes, it 
has always been a mooted question as to whether the vascular lesion or 
direct bacterial action is responsible for the gangrene. 

In gas phlegmon blood vessel lesions have been regularly encountered. 
Some authors have described a fatty degeneration of the vessels and a prolifer¬ 
ating endarteritis with gas gangrene. Legros describes also an obliterating 
endophlebitis. Inasmuch as the entry of the bacteria into the blood vessels 
has not been demonstrated, it is believed that the lymphatics are invaded and 
possibly the capillaries, the latter portal of entry explaining the bacteriemia. 

Bacteria, however, have been shown to enter the vein walls, in gas gangrene 
when the bacilli of malignant edema are associated. 

Period of Incubation. —Since the gas bacillus can vegetate in the wound 
for some time, the period of incubation varies. As a rule, manifestations 
appear within the first four days. 

1 Welch and Nuttall, Bull, of the Johns Hopkins Hosp., 1892, 3, 81. 


13 


194 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


According to Hancken 1 the gas phlegmon appears on the first day in 21 per cent, on 
the second day in 33 per cent; on the third day in 15 per cent; on the fourth to the slx th day 
in 4 per cent; on the seventh to the eighth day in 3 per cent, and from the eleventh to 
the twentieth day in 1 per cent of the cases. Of 119 cases studied by Franz 2 gas. for¬ 
mation was noted 29 times within the first two days; 18 times after three days, 14 times 
after four days. 

Occasionally there is a very short period of incubation no longer than a 
few days after injury. It is said by certain authors that infection may be 
carried through field hospitals, through kitchen utensils, dishes and instru¬ 
ments. This is doubted by others. For it is known that war wounds 
often harbor anaerobic organisms that remain dormant for weeks or months, 
and then by reason of subsequent tissue injury light up and become activated. 

Latent Infection with Anaerobes .—It is believed (Melchior) that organisms of this type 
may be buried for a long time even in healed wounds and become active after weeks or 
months. This has been shown to be the case with the tetanus bacillus, 3 when buried 
bullets or shot fragments are removed from old scars and the symptoms of tetanus develop. 
The spores of the tetanus bacillus are said to remain for a long time in the scar and are 
activated and made virulent through the trauma of operation. Similarly, gas bacilli can 
be reactivated. Indeed Wieting 4 reports a gas phlegmon following grenade wound with 
healing. Six months later, after an attempt to remove the imbedded metal, gas infection 
occurred with a lethal outcome. Enough cases in which the primary wounds had already 
healed with good cicatrization have been described to confirm the correctness of such 
observations (Melchior, 5 Kiittner, 6 Hodesmann 7 ). 

Pathogenesis of Gas Gangrene .—It has been said that the majority of all 
war wounds contains anaerobes. Bacteriologists working in the neighbor¬ 
hood of the battle fields have found gas bacilli in a large percentage of wounds 
during the Great War, though no clinical manifestations were present. Even 
in ordinary infected wounds gas bubbles were not infrequently seen, so that 
from the practical standpoint it must be accepted that almost all of the 
wounds contain gas bacilli. This does not signify however, that all wounds 
become gas phlegmons, inasmuch as special factors must be present to facilitate 
the activity and develop the virulence of the anaerobes. 

Two additional factors, namely, earth infection and special wound con¬ 
ditions are necessary. Entrance of earth carries with it anaerobes that have 
been derived from the excreta of animals. Such earth is carried there by 
hand grenades, fragments or even when pieces of clothing are carried in by 
bullet shots. 

The bad wound conditions referred to include laceration, contusion, 
extensive compression and detachment of tissue fragments with tearing of 
vessels and circulatory insufficiency of the wound. Anaerobic organisms 
develop rapidly in the necrotic tissue. The leucocytic poisons elaborated 
and the negative chemotactic reaction induced by the organisms explain the 
absence of the usual cellular exudate. 

The Incidence of Gas Gangrene. —Amongst the wounded in the late 
war, gas symptoms are said to have occurred in the following frequency. 
Wieting 3-5 per cent, Marwedel 8 2.8 per cent, Rumpel 9 3 per cent and Franz 10 

1 Hancken, Feldarztl. Beil. z. Miinchen. med. Wchnschr., 1916, 1030 (462). 

2 Franz, Deutsch. med. Woch., 1917, 39, 1220; also Bruns Beitr. z. klin. Chir., 1917, 
106, 443; also Deutsch. med. Wchnschr., 1917, i 4 > P- 446 . 

3 Buerger and Heimann, Am. Jour. Med. Sc., Aug. 19, 1905. 

4 Wieting, Deutsch. Ztschr. f. Chir., 1917, I 4 I > i- 

5 Melchior, Berl. klin. Wchnschr., 1915, 5, 97 - 

6 Kiittner, Bruns’ Beitr. 103, 300, 1916. 

7 Hodesmann, Deutsch. med. Wchnschr. 1917, 22, 687. 

8 Marwedel, Feldarztl. Beil. z. Miinchen. med. Wchnschr., 1915, 30, 1023, 479. 

9 Rumpel, Samml. klin. Vortr., 1917, 736, 39, 329. 

10 Franz, Bruns’ Beitr. z. klin. Chir., 1917, 106, 443. 


MICROBIC GANGRENE 


195 


2 per cent. Where hand to hand battles occur gas bacillus cases are frequent; 
also where rescuscitation facilities are poor and wounds are neglected. 
During the wet period with considerable rainfall, cases are more frequent 
than in dry periods, probably due to the wetting of the clothes and accumu¬ 
lation of anaerobic organisms in clothing already soiled with earth. 

It was by far more prevalent while fighting took place on the well ferti¬ 
lized fields of Belgium and France, than in the mountainous regions of the 
Italian and neglected forests of the Russian fronts. 

Localization of Gas Gangrene. —In view of what has been said, gas 
gangrene must be expected in those portions of the body where muscle tissue 
is present, particularly where large muscle masses occur, namely, in the 
extremities. Thus, the lower extremity is more frequently affected than the 
upper (2^ times). It occurs in the trunk, where there are large muscle 
planes; but rarely is it found in the region of the head and neck, infrequently 
affecting the foot and hand. It may be multiple, implicating more than 
one extremity. 

The cases in which gas phlegmon of the brain occurred are not due to the 
organisms described here, and doubtlessly are the result of extension from 
head wounds containing anaerobes. Gas gangrene of bones does not occur, nor 
of the abdominal organs. Reports of authoritative cases of gas infection of 
the liver have not been forthcoming, and the spongy liver reported at some 
autopsies (Schaumleber) must be regarded rather as a postmortem process. 

Types of Gas Gangrene Infection. —Epifascial gas phlegmon of more 
benign nature has been differentiated from the malignant subfascial form 
(Payr 1 ). The former usually heals after multiple incisions; the latter is 
fulminating, converting the muscle into a pasty mass; the extremities die off 
and require amputation or exarticulation to save life. The deep form of 
infection corresponds to the gas gangrene and gas phlegmon of other authors 
and is well accepted. The superficial form is regarded as a less virulent type 
of infection, and is thus described. 

The Superficial Form .—Its seat is between the skin and fascia, the muscle 
being uninvolved. The skin is edematous and shows deep orange or almost 
coffee colored patches. The subcutaneous tissue is infiltrated with amber 
colored fluid; the skin may show blebs; and subcutaneous crepitation due to 
gas can be elicited. The fascia is not necrotic, but the underlying muscle 
seems to be healthy. The general systemic condition shows marked disturb¬ 
ance, with fever and rapid pulse; but the prognosis is good. Some authors 
(Bier 2 ) refuse to accept this type as being one of true gas phlegmon, believing 
that the epifascial form of Payr is also a muscle disease due to infection of a 
bullet wound and represents an extension of a deep focus, one of such slight 
virulence as to give the above described manifestations. It is noteworthy 
that true gas phlegmon does not occur after bullet wounds that fail to 
implicate the musculature. 

In short, according to some the epifascial form may be regarded as a mild 
distribution of this infectious process in superficial planes, and arising from a 
primary deeper focus. It differs from the true gas bacillus infection, in that 
it usually yields promptly to conservative treatment with multiple incisions. 

Summarizing the types of gas infection we may speak of the following: 

First, local gas phlegmon which is benign and has no tendency toward 
unlimited extension, but localizes itself involving single muscles. 


1 Payr, Munchen. med. Wchnschr., 1915, 57; also Med. Klin., 1916,442. 

2 Bier, Med. Klin., 1916, 14, 355. 


196 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Second, progressive gas phlegmon which is malignant, in that muscle disin¬ 
tegration may extend over the whole of a portion of the body (member) and 
usually ends in gangrene; and 

Third, anaerobic sepsis which extends rapidly without bounds, is attended 
with severe general symptoms, and terminates fatally. 

A. The Toxins of Gas Gangrene—The general symptoms correspond well to the clinical 
picture of a severe poisoning, the toxins being partly of bacterial, partly of tissue origin. 
The question of the development of a true toxin from the gas producing organism is a 
mooted one as regards the Frankel-Welch bacillus. However, in the case of the bacillus 
of malignant edema, true toxins have been demonstrated (Ficker*), the intravenous injec¬ 
tion of very small quantities of which, produces a lethal effect in rabbits. This finding 
would lead to the expectation of appropriate serological treatment. 

According to Wassermann 1 2 all gas bacilli produce a similar poison, just as staphylococci 
produce a staphylolysin, so that this author believes that the poison is derived rather 
from degeneration of the bacterial bodies, than from products of their action. 

Clinically, however, there seems to be evidence in favor of the elaboration of a bacterio- 
genic blood poison. Indeed, one that attacks the hemoglobin of the blood. The Frankel- 
Welch bacillus, also the Aschoff, have a lytic effect on the red blood cells. Other authors 
(Kamen 3 ) speak of a toxin with a specific action against the leukocytes (leukocidin), 
in addition to the active, negative chemotactic action of the poison. The most injurious 
effect of the bacillary poison is the chemical action on the hemoglobin, which is liberated 
from the red blood cells, and converted into methaemoglobin. Hemoglobin, therefore, 
appears in the blood serum and in the urine. Clinically, this action has been observed in 
puerperal processes, and an attempt made to correlate the brownish, cyanotic skin color, 
air-hunger, and a brown blackish appearance of the urine, with the production of the 
hemoglobinaemia and the hemoglobinuria. Such severe disturbances in the blood, however, 
have not been observed in gangrenous processes, but rather in the puerperal. Enough data 
has been forthcoming to confirm the theory of the existence of a toxin. The yellowish and 
brownish spots of the skin have been regarded as due to hemolysis, and the marked icterus 
in the lethal cases, as due to the rapid degeneration of blood cells. 

The histogenic poisons developed locally have not been thoroughly studied. It has 
been shown that autolysis of tissues produces a poison, and here the muscle tissue in its 
degeneration might be considered as the origin of a toxin. The symptom of marked collapse 
has been due to anaphylactic shock. As the muscle protein breaks down through the pep¬ 
tonizing action of the bacilli, toxalbuminates or foreign body proteins are absorbed, cause 
hypersensitization and anaphylactic symptoms. Furthermore, acids—carbonic, lactic, 
butyric, propionic, etc.—as they are formed in the process, are said to irritate the respira¬ 
tory centers, and produce Kussmaul’s type of breathing. 

General Symptoms. —In the severe cases of gas gangrene the general 
symptoms are marked, collapse being an early sign of a rapidly progressing 
gas gangrene. The face has peculiar pale appearance, whilst the tongue 
remains moist. The pulse becomes very rapid, so that a frequency of 140- 
160 is not unusual. The blood pressure sinks rapidly, the lips become cyan¬ 
otic. Striking changes in respiration are noted, often of the Kussmaul type, 
similar to that of diabetic coma. Dyspnoea with the employment of all the 
accessory respiratory muscles is characteristic, due to central irritation of the 
respiratory center. This manifestation has been explained on the assump¬ 
tion that acids elaborated in the gangrenous process are absorbed, or that 
bacteria produce carbonic acid in the blood itself (Pribram) that acts directly 
upon the respiratory center. 

The temperature is not usually high, may be normal or subnormal, and 
it is only when there is slow development of gangrene that there is elevation. 

Icterus is a dangerous and grave manifestation, an indication of anaerobic 
sepsis, and that the hemolytic process is making itself manifest in the circu¬ 
lation. The assumption that liver changes are responsible does not seem 

1 Ficker, Med. Klin., 1917, 45, 1181. 

2 Wassermann, Med. Klin., 1916, 17. 

3 Kamen, Zentralbl. f. Bakteriol. Parasitenk. u. Infectionskr., 1904, 35, 554-686. 


MICROBIC GANGRENE 


197 


tenable, in view of what has been previously said regarding liver lesions. 
Vomiting and singultus are often associated with the icterus. Marked 
hyperhidrosis is striking. 

The blood picture very soon becomes altered, the hemoglobin being diminished, and the 
erythrocytes showing the picture of anemia with marked anisocytosis (macro- and micro¬ 
cytes). The white blood cells show changes, there being eosinophilia and leukopenia. 
The absence of increase in the number of neutrophiles is said to be characteristic for gas 
gangrene. The blood picture persists even after convalescence for a considerable period 
of time, with a marked anaemia, poikilocytes, polychromasia and megalocytes. 

There is diminished coagulability of the blood. The urine contains 
albumin, granular casts, often blood. 

All of these symptoms may be present with complete conservation of 
consciousness. Often euphoria is noted, and the picture is not unlike that of 
poisoning by serpent venom, and sometimes of pancreas necrosis, all being 
manifestations of severe intoxication. 

Local Symptoms. The Wound .—Where the wound is wide open, the 
musculature becomes dark, blackish and crepitates, and the uninvolved 
muscles are glassy by reason of extensive infiltration with edematdus fluid. 
Gas bubbles glitter here and there like pearls in the tissue. The skin edges 
become necrotic. The absence of inflammatory reddening and heat is charac¬ 
teristic. When it is present, it is due to mixed infection. The fluid of the pure 
cases of gas bacillus infection is serous or resembles laked blood filled with 
bubbles of gas. Swelling and pain are always present, the result of collateral 
edema. The regional glands are not enlarged. 

The Skin .—Where the process is developed in the depth, the skin is at 
first but little involved. Often, over the muscle focus, the integument has a 
white, glistening, swollen appearance, in which the dilated veins are promi¬ 
nent. When the gas formation approaches the skin, characteristic changes 
appear, namely, a brownish or orange colored patch, or bluish or violet areas 
of discoloration. With the former there may be blebs with watery or yellowish 
fluid, that are distributed in geographic figures or discrete fashion. In the 
region of the brownish spots, the skin may undergo a leather-like necrosis, 
and an incision into it evokes no bleeding. Where the bluish discoloration is 
present, the gangrene is more intensive, the skin dies off rapidly together with 
large parts, or the whole of the extremity. Such blue patches are always 
the precursors of total necrosis and gangrene involving all the layers. The 
brownish patches indicate more limited necrosis often only of the skin. 
When patches of skin are sequestrated, secondary infection with suppuration 
may take place. 

The Gas Formation .—This is the most characteristic symptom, being the 
product of the breaking down of the muscle carbohydrates and the decompo¬ 
sition of proteins. This accumulation of gas may be so enormous, and its 
migration so distant that when the lower extremity is involved, gas bubbles 
are said to have travelled into the subcutaneous tissues of remote parts. The 
distension may be so great that incision into the skin gives rise to a blowing or 
puffing sound. Palpation or percussion suffices to detect the presence of 
gas. X-ray examination shows free gas in the tissues. In the picture, spots 
or streaks between the muscle and into the subcutaneous tissue can be visual¬ 
ized, in territories far removed from the bullet wound. 

The Edema .—Usually marked edema accompanies gas production, and is 
responsible for the appellation “gas edema.” The places vary, according to 
reports, some having marked gas production without gas edema, others marked 
edema without gas. The edema of gas gangrene is rather characteristic. It 


198 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

is of yellowish color or serous, causing marked bulging of the subcutaneous 
tissue, and muscular interstices and vascular sheaths. This is very striking 
about the sciatic nerve. The edema can become brownish due to blood 
admixture. Two views as to the significance and purpose of the edema have 
been suggested. According to one it is defensive and tends to combine and 
nullify the action of the toxins and lytic products. According to other views 
the edema has a contrary function, namely, in that it contains aggressins 
which are toxic for the cells of the body. As such it would assist the bacterial 

action as an advance guard. . 

The Gangrene .—This should be described under the classification ot mlec- 
tious gangrene, being the direct clinical expression of the action of certain 
bacteria. Gas gangrene, occurs directly in the infected wound, and not at the 
termination of an extremity. In this way it differs from the gangrene that 
results from injury of important vessels. The necrosis begins in the muscle. 
The action of the bacilli and the development of gas produce a pale red 
discoloration of the muscle which gives way to a darker color. FinaLy, as 
fluidification takes place, a chocolate porridge-like mass is formed. All the 
individual muscles are not equally affected, so that on cross-section, at ampu¬ 
tation, or autopsy, the mottling with the contrasted involved and non- 

involved groups is striking. . 

From here the gangrene extends into the external skm which becomes 
bluish or violet in color, and then grayish black. The epidermis is lifted off 
with the formation of bloody blebs, and the process extends more rapidly 
peripherally than centrally. 

When the gas necrosis surrounds the limb so as to involve all the circu¬ 
latory channels, the peripheral parts show evidences of impaired circulation, 
in absence of pulse, anemia, and coldness. In this way a secondary anaemic 
gangrene of the peripheral portions of the extremities may result because of 
poor nourishment. These two processes, therefore, may meet and become 
confluent, one descending, the other ascending. 

The process of mortification may be so rapid as to implicate a whole limb 
within a very few hours, and is due to the enormous rapidity of the multi¬ 
plication of the organism. Thrombosis of the large veins may add to the 
rapidity of the mortifying process. Some authors attribute the fulminating 
form of gangrene to the contractile effects of the toxins on the vessels; others, 
to the accumulation of products that cause necrosis by pressure. 

Vessel Injury and Gas Gangrene— When large vessels of an extremity are injured bv 
bullet wound, or when it becomes necessary to ligate large vessels such as the popliteal 
because of hemorrhage, the liability to gas gangrene infection is already present and the 
progress of such infection is greatly enhanced. Thus, after ligation of the popliteal during 
the Great War, it was observed that gas infection developed frequently, necessitating ampu¬ 
tation. Of 39 cases studied by Bier and Specht 1 in which amputation for gas gangrene 
was necessary, there were 33 in which injuries to the large arteries had occurred. Accord¬ 
ing to some authors, however, the gas formation is a secondary process, consequent upon 
the arterial thrombosis, when anaerobic, saprophytic organisms multiply in the dead tissue. 

Clinically, however, it is difficult to differentiate the two types, and it must be accepted 
that circulatory disturbances are an important factor in predisposing to anaerobic infection. 

Diagnosis. —In severe cases the diagnosis is easy. The so-called anaer¬ 
obic sepsis is characterized by the altered breathing, the deep collapse, 
the weak pulse, with conservation of consciousness. The progressive gas 
phlegmon with its edema, emphysema, foul odor, discoloration of the skin, 
the gangrenous change of the muscle tissue, the peculiar pallor of the face 

1 Bier and Specht, Bruns’ Beitr. z. klin. Chir., 1916, 101, 271. 


MICROBIC GANGRENE 


199 


with the poor general condition—all these are characteristic manifestations. 
Severe pain often initiates the onset of the process, and when it occurs, a few 
hours or a day after the injury, is a premonitory sign of significance. When 
in doubt, an incision is indicated which may bring to light the peculiar 
change in the muscle, or possibly even gas. Severe streptococcus phlegmon 
may also produce gangrene of the extremity, but gas is not present, nor is 
there a characteristic sound on percussion. 

Morbidity and Mortality.—Early in 1918, Gross 1 had 2,796 wounded men pass through 
his hands, of whom 101 (3.6 per cent) developed gas gangrene. Late in 1916 he treated 
1,676 wounded men, 2 33 of whom (1.9 per cent) developed gas gangrene. In October, 
1918, Sieur and Mercier 3 reported that fewer than 0.5 per cent of the wounded developed 
gas gangrene in the advanced and intermediate zone. This was undoubtedly due to 
improved hygienic conditions and character of the soil (non-fertilized). Lardennois 4 
in 1916 reported 500 cases of gas bacillus infection with 15 per cent mortality; and Ivens 8 
in 1917, 460 cases with 9.5 per cent mortaity. 

Regarding definite gas gangrene as distinguished from gas bacillus infection in general, 
Gross, in 1916, listed 101 cases with 56.5 per cent mortality, while Ivens, in 1917, reported 
107 cases with a mortality of 26.4 per cent. It must be emphasized here, however, that of 
the cases reported by Gross, those which were treated within twelve hours after the wound 
was received had a mortality of only 10.9 per cent. This indicates more clearly than any 
description could, the importance of early treatment. 

Treatment.—The general principles include the following: detoxication 
by serum; control of shock; the intravenous injection of sodium bicarbonate 
for acidosis; the early and thorough removal of all injured tissues, infectious 
agents and foreign bodies by surgical intervention, although it is not always 
necessary to remove large areas of skin and subcutaneous tissue. All sutur¬ 
ing is to be avoided; free drainage is to be instituted; the proper splints 
applied; and Carrel-Dakin solution used. The question of amputation 
depends on the condition of the patient, the extent of infection, its proximity 
to the body and whether or not the infection can be controlled by conserva¬ 
tive measures. 

For the collapse symptoms hypodermic stimulants, hypodermoclysis, 
intravenous injection of glucose solution (5 per cent), subcutaneous injections 
of adrenalin and salt solution are indicated. In view of the hypothetical 
assumption that the systemic manifestations represent the effects of acid 
intoxication, subcutaneous soda solution per cent) and intravenous 
administration have been followed by definite results. Hypertonic solution of 
salt intravenously injected is also recommended (Hercher, introducing 
sodium chlorid 8.5, potassium chlorid 0.3, calcium chlorid 0.3 with water 
up to 100). 

Van Beuren gives the following general rules used for treatment of gas bacillus infection 
during our recent war. First, operate as early as possible. Second, use nitrous oxid- 
oxygen anesthesia if possible. Third, prepare the part with the minimum amount of delay 
and trauma. Fourth, avoid tourniquets. Fifth, make incisions longitudinally and half 
again as long as you think they need be, both in the skin and fascia. Sixth, leave as much 
skin as you dare in your debridgement. Seventh, go between, rather than through, normal 
muscles, and do not cut across them unless you have to (better a long separation between 
two than a short cut across one). Eighth, however open the wound as thoroughly and 
freely as you possibly can. Ninth, excise all torn, crushed, discolored, noncontractile 
muscle, until you have left only that which is firm, of normal color, actively contractile, and 
which bleeds readily. Tenth, make a careful and conscientious search for and remove all 
loose bone and foreign bodies, especially clothing and blood clots. Eleventh, stop the 

1 Gross, G.-Bull. de l’Acad. de med., Dec. 26, 1916, 76, 586. 

2 Gross, G.-Bull. et mem. Soc. de chir. de Par., 1917, 43, 636. 

3 Sieur and Mercier, Bull, de I’Acad. de med., Oct. 29, 1918, 80, 394. 

4 Lardennois and Baumel, Presse med., Nov. 16, 1916, 24, 506. 

5 Ivens, Med. Press & Circular, 1917, 103, 12. 


200 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

bleeding; leave the wound wide open and separate its walls with wet gauze, laid in, not 
packed in. Twelfth, use Carrel-Dakin tubes, if you know they will be properly cared for, 
otherwise omit them. Thirteenth, use plenty of dressings and make careful splint fixation 
of the part. Fourteenth, do it all as rapidly as you possibly can. 

We may divide the treatment into surgical treatment, treatment by 
hyperemia, by oxygen insufflation, medical treatment, transfusion of blood, 
and serum therapy. 

Surgical Treatment—In the mild cases of local gas phlegmon, wide and 
extensive incision are the most reliable means for establishing a cure. The 
incisions must be carried well into the healthy tissues, until bleeding muscle 
is reached. This is to be followed by loose tamponade drainage, the use of 
Carrel-Dakin solution and splinting, to secure adequate repose of the parts. 
When we can detect more extensive infiltration of the interstices of the muscle 
with gas and edema’, when the vascular sheaths are involved, and the process 
is recognized in the discoloration of the skin, and subcutaneous emphysema 
the excision must be carried along such planes as seem to be involved, along 
the vessel sheath and through the skin. The incisions through the skin are 
best made in multiple fashion. 

Where the affection is more virulent, and shows marked progressive 
tendencies, more radical means are resorted to. So certain authors recom¬ 
mend instead of the longitudinal incision (Fessler 1 andFriind 2 ) transverse 
incisions, which enable a more adequate and accurate investigation of the 
muscle masses to be made. Indeed, in very bad cases, it may be necessary 
to excise whole muscular territories. 

When the gangrenous process threatens to invade the opposing groups of 
muscles, to encircle the bone and to creep over the joint immediately above, 
amputation is in order. The well developed gangrene of a portion of a limb 
is also an indication. Should severe fractures through bullet wound (of the 
long bones) complicate, amputation is also recommended. Even when the 
gangrenous process is not as yet in evidence, but when the general symptoms 
are severe, with rapid and weak pulse, threatening collapse, ablation of the 
limb must be considered. 

It is best to ablate in healthy tissues, at least beyond those macro- 
scopically involved and beyond the edema, although cases have been reported 
as cured where the amputation was very near and even through diseased 
parts. In very extensive cases, exarticulation may be necessary. This 
procedure is not so dangerous when done through the shoulder and gives 
good operative results. A similar operation through the hip, however, is a 
dangerous surgical procedure with a high mortality. 

Lawson 3 believes that the best results can be obtained by treatment of the 
subcutaneous tissues with nascent oxygen in the form of injections of neutral 
hydrogen peroxide. Infiltration of the healthy tissues with oxygen above the 
line of spreading gangrene is sufficient to check the advance of the infection, 
and in the majority of cases, the limb may be saved. He believes that ampu¬ 
tation of the limb for acute emphysematous gangrene is unnecessary, unless 
all of the tissues are involved over an extensive area, thinking that high 
amputation may prove fatal from shock. 

Treatment with Hyperemia .—This includes active hyperemia and con¬ 
gestive or obstructive (Stauung). 

1 Fessler, Feldarztl. Beil. z. Munchen. med. Wchnschr., 1917,10,331. 

2 Frund, Bruns’ Beitr.,1916, 98, 447. 

3 Birm. Med. Rev., 1915, LXXVIII, p. 67. 


MICROBIC GANGRENE 


201 


Obstructive Hyperemia. —Bier recommends the rhythmic method, claim¬ 
ing good results. When the usual method is employed, 22 hours application 
and 2 hours interruption are not recommended. Although these methods 
have been well developed on the Continent and particularly in the Central 
States, they have found but few adherents in America. 

Oxygen Insufflation. —Because of the danger of oxygen embolus, this 
method has not won many supporters. It had been recommended in the 
form of insufflation into the tissues. Intramuscular injection of 3 per cent 
hydrogen peroxide has also been suggested with a fatal result (Borscher). 

Local Medication. —Various types have been used, such as the washing 
with peroxide, and Dakin’s solution. Charcoal has been used with a view to 
combine with the aggressins formed by the bacteria. None of the local 
methods of treatment have had worth-while results. 

Blood Transfusion. —Both as a prophylactic measure before amputation 
or after this procedure, blood transfusion is exceedingly valuable. It is 
worthy of a trial for its beneficial effects in combatting the toxic results 
of infection. 

Serum Therapy. —For the elaboration of a dependable serum, it is 
necessary to employ something that not only has an antitoxic function, but 
also is anti-infectious, in the sense that it can inhibit the enormous multi¬ 
plication of the organisms in this disease. The existence of both histogenic 
and bacterial poisons, as a result of the action of the bacteria, makes it hard 
to find an appropriate serum. 


An antibacterial serum was prepared by the firm of Hoechst which is a polyvalent, 
antibacterial, immune serum procured from horses. In the production of it, the Frankel- 
Welch group, the gas edema group and the putrificus group were employed. _ It was given 
a trial during the Great War in doses from 20-40 cc. Rumpel injected it locally, just 
central to the wound; he also tried intravenous application. His results were considered 
satisfactory in that the mortality was reduced. Anaphylactic symptoms appeared only in 
a few cases. Aschoff compares a mortality of 43.9 per cent in the cases in which the 
Hoechst serum was used, against a mortality of 68.7 per cent without any. Weinberg 
and Seguin employed an antitoxic and bactericidal serum including the following group- 
bacillus perfringens (Frankel-Welch), sporogenes, cedematicus, vibrion septique and bacillus 
hemolyticus (Weinberg and Seguin). 1 

Statistics on the efficacy of anti-gas bacillus serum are somewhat meagre, but are on the 
whole favorable. Elser advises the following routine for serum treatment. 

1. A prophylactic dose of polyvalent serum, given as early as possible after the receipt 
of the wound, combined with tetanus antitoxin. 

2. Bacteriologic examination of the wound and establishment of the presence of gas 
bacillus infection and determination of the variety of the bacteria. The determination 
can be made in about 24 hours. 

3. Administration of the specific serum, either single or polyvalent or “pooled,” accord¬ 
ing as there are one or more gas formers found and also antistreptococcus serum. 

Sacquepee 2 recommends the following procedure for differentiation to determine the 
type of anaerobe present. 

In each of four test tubes is placed 1 cc. of macerated gangrenous tissue and to three 
tubes respectively is added 1 cc. of each of the three antiserums. After incubation for half 
an hour the contents of each tube is injected respectively into one of four guinea pigs. The 
one protected by the serum shows no reaction. The others die. They usually become sick 
in from 6 to 12 hours. 

The various reports generally agree that intravenous injection (while not always 
possible) is to be preferred, in combination with deep muscular injection, proximal to, but 
in the vicinity of the wound. 

Dosage: 5-15,000 units of specific or pooled serum intravenously to be repeated in 2 
hours if no improvement occurs. At the same time, an equal amount is given intramus¬ 
cularly in divided doses. This can be repeated in 24 hours, followed by daily injections. 

1 Weinberg and Seguin, Miinchen med. Wchnschr., 1917, 152 and 848. 

2 Sacquepee et de la Vergne, Bull, de l’Acad. de med., 1919, 506. 


202 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Anaphylactic reactions are rare. It is emphasized that sero-therapy is entirely auxil¬ 
iary, and in no way replaces operative treatment of wounds. The time of application 
should be as early as possible, since it is practically useless when the infection reaches the 
stage of septicemia. 

Gangrene Due to Pyogenic Bacteria.—The role of this type of organism 
in causing tissue mortification has not been carefully studied so that we 
can but dwell superficially on this theme. Enough is known, however, to 
permit of the conclusion that streptococci of various types, and other organ¬ 
isms when virulent, or in symbiosis, are able to cause extensive local tissue 
disintegration in a direct fashion, or in a secondary or indirect way by virtue 
of thrombosis induced locally in arteries and veins. 

The direct alterations in some of the streptococcal forms are of a destruc¬ 
tive type and are quite different from the usual purulent lesions. The skin 
of the affected region may rapidly take on a yellowish, brownish or bronze 
color, a significant appearance in these virulent infections. 

The secondary gangrene of parts in or distal to the infected area, is often 
of the dry type when digits are involved and due to a contiguous thrombotic 
process in larger arteries and veins. 

Dry gangrene of one or more phalanges may follow rapidly in the wake of 
a severe infection of the palmar sheath, with or without infection of the 
dorsum of the hand. Streptococcus hemolyticus is the more common offend¬ 
ing agent. Dry gangrene of the fingers or toes may rapidly ensue, hnd is 
probably due to thrombosis of the digital vessels at the base of the finger. 
It is secondary in the sense that it is one of the complicating effects of the 
infection on the larger source of blood supply. Therefore, it is not a necrosis 
of tissue due to the direct action of the organisms as is the case with many of 
the anaerobes. Extensive direct necrosis may here, too, be due to the bac¬ 
terial influence. 

The clinical course, which was well exemplified in one of the author’s 
cases recently observed, may be briefly summarized as follows: 

Severe infection apparently located in the palmar sheath of the index finger with 
lymphangitis extending up to the elbow and above, and temperature of 104° for about one 
day before the patient was seen by the author. Two small median incisions over the palmar 
surface of the first and second phalanges liberated turbid fluid from the tendon sheath. 
Another small incision over the dorsum within the zone of lymphangitis,. permitted the 
same type of fluid to escape. Within twenty-four hours following this incision, the lymph¬ 
angitis had extended to the axilla, and the following condition of the hand required 
further operative procedure. The dorsum was evidently the seat of an extensive strepto¬ 
coccus infection, and the palmar infection had spread to about three quarters of an inch 
farther down into the palm. The two distal phalanges of the fore-finger were bluish black 
and gave all the signs and had all the appearance of an early stage of gangrene. 

Multiple incisions were made over the dorsum of the hand, draining a large amount of 
purulent fluid that had collected within twenty-four hours, and the palmar incision was 
carried three quarters of an inch farther down into the palm. By these incisions the infec¬ 
tion was controlled, so that no further operative intervention was necessary. However, 
the two distal phalanges became rapidly mummified. 

Here we may assume that the streptococcus infection (streptococcus 
hemolyticus in pure culture) was of such virulence as to cause contiguous 
thrombosis in the digital arteries, and mortification of the two distal 
phalanges. 


GANGRENE COMPLICATING INFECTIOUS DISEASES 


203 


CHAPTER XXXV 

GANGRENE COMPLICATING INFECTIOUS DISEASES 

Typhoid Fever.—Recent authors (Klose 1 ) have called attention to the 
twofold causal elements that occasion vascular symptoms in the course 
of typhoid fever, namely: The injury to the walls of the peripheral vessel, and 
a central specific affection of the vasomotor center. 

When the larger arteries are involved, thrombosis, hemorrhage and 
gangrene occur; and the bacilli or their toxins may simply increase the 
permeability of the capillary endothelium, and bring about edema and 
transudates. 

Hyaline thrombus formation resulting from parietal infectious injuryv 
of the vessel wall, with stenosis of the vessels and localized circulatory distur¬ 
bances are reported. Corresponding to these changes we encounter the com¬ 
plication of typhoid fever, namely, hemorrhages into the various organs. 

The larger arteries are described as containing foci of degeneration and 
inflammation. Involvement of the cerebral arteries is reported in the litera¬ 
ture (Jaffe 2 ). 

Gangrene of the peripheral parts of the extremity may be the issue. 
External causes such as cold, and the chemical factors predispose to and 
increase the severity of the gangrene. Necroses of the feet, fingers and 
forearm, the genitals and nose have been reported. These were rather 
common complications in the Great War, when toes were usually found 
involved, although in certain cases, gangrene extended to the ankle or 
higher. Sometimes it was symmetrical or multiple. Usually operative 
intervention became necessary. 

A prodromal stage is characterized by intense paraesthesiae and pain, and 
sensory disturbances in the affected extremities. The pain may last for 
weeks, and may be attended with pallor and a marmorated appearance of 
the skin before gangrene appears. The latter may attend the early part of 
the clinical course, or after the temperature has attained the normal. 

In infection with the paratyphus bacillus, mycotic aneurysms may develop. 
When these are situated in the vessels of the extremities, circulatory dis¬ 
turbances may result. Gangrene of the forearm was barely averted in a 
case (Sick 3 ) in which a mycotic aneurysm was located at the bifurcation of 
the brachial artery. 

It has been assumed that bacterial emboli entering the vasa vasorum are 
responsible for the vascular lesions. 

Gangrene in Recurrent Fever.—Symmetrical gangrene of the toes is one 
of the complications of this affection. In some cases circulatory disturbances, 
pain and cyanosis of the skin may precede the necroses. Perhaps in addition 
to the action of the spirochaetes, external factors such as cold may be con¬ 
tributing causes. 

For further consideration of gangrene complicating infectious diseases, 
the reader is referred to Chap. LXXVI on Acute Arteritis. 

1 Klose, Ergebn. d. Chir. u. Orth., 1921, 13, p. 74. 

2 Jaffe, Med. Klin., 1918, nos. 9, 22, 23, 24. 

3 Sick, Munchen. med. Wchnschr., 1918, p. 237. 


204 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XXXVI 

INJURIES TO THE BLOOD VESSELS AND GANGRENE 

The traumatic lesions of the blood vessels may be described as including 
firstly, recent injuries; secondly, pseudo-aneurysms or that type which has 
been described as pulsating hematomata; and thirdly, well developed 
aneurysms. 

Recent Injuries.—Statistics (Stich) taken from the Great War show wide 
variations; but in the armies of the Central Powers from 40 to 45 per cent 
of all injured, suffered vessel lesions. Not more than one-half of those who 
received bullet wounds of the vessels arrived alive at the hospital stations. 
Often spontaneous cessation of hemorrhage takes place, especially if of venous 
origin. Injuries of the veins from bullet wounds are more common than 
those of the arteries. 

A knowledge of vein injuries is important, in that these may lead to remote 
functional disturbances, even though the immediate effects do not seem to 
be threatening. Indeed, the functional disturbances that follow may last 
for years, while the cause thereof may be wholly over-looked. 

Even bullet wounds of the arteries may cease to bleed spontaneously. If 
these facts are taken into consideration, the incidence of vessel injury is in all 
probability greater than statistics would show. 

Bullet wounds of the peripheral arteries most frequently involve the 
femoral and popliteal; wounds of the axillary and brachial arteries are some¬ 
what less common. 

Pathology.—The character of the vascular lesions would depend to a cer¬ 
tain extent upon the character of the shot. Large grenade fragments or 
shrapnel may occasion the severest tears. When the pieces are sharp the 
vessels may be incised as if with a knife, and abundant bleeding ensue. 
Tangential trauma may produce contused wounds and holes; or large vascu¬ 
lar wounds may result with consequent retraction of the distal and proximal 
ends of the artery. In the latter instance, bleeding may be but minimal. 
^/li infection does not take place, thrombus formation and organization 
follow. The smaller vessels are usually torn through the action of infantry 
bullets. In the larger vessels, the same shot causes extensive destruction, not 
only by direct action, but by the secondary impact and penetration of con¬ 
tiguous or nearby bony splinters. Circular and also slit-like orifices are 
occasioned, the latter frequently being smaller than the caliber of the bullets. 

The blunt forms of traumatism produce there types of injuries; (1)total 
tearing with complete interruption of the continuity of the vessel; (2) partial 
rupture with lateral injuries; and (3) rupture of the intima and media with 
intact adventitia. Such lesions less frequently occur in the veins, but the 
latter more often are injured in the neighborhood of comminuted fractures. 

Injuries Due to Treatment .—Vascular injuries sometimes follow joint dis¬ 
locations. More important are the observations concerning injuries to 
vessels in sequence of orthopedic attempts to correct position in old 
dislocations. 

The author recently had occasion to see a young woman in consultation, in whom the 
femoral artery was torn in an attempt to correct an old ankylosed hip. Five days after the 
injury, the greater part of the foot was in a state of gangrene; all the usual palpable arteries 
of the extremity failed to beat, and there was an enormous hematoma occupying the 


INJURIES TO THE BLOOD VESSELS AND GANGRENE 


205 


inguino-femoral region, with brawny sanguinous infiltration of a large part of the upper and 
inner aspects of the thigh. Spontaneous cessation of the hemorrhage had occurred by the 
pressure hematoma. 

As many as 20 such observations are recorded by Korte in dislocated shoulders. 
Complete tears, as well as lateral holes, have been observed, and in 3 autopsies injuries of 
the veins are reported. The factors responsible for the ruptures, were the employment of 
excessive force, abnormal friability of the vessels, adhesions of the vessel sheath with the 
contiguous bone or joint capsule or simultaneous fracture of the head of the bone (femur or 
humerus). 

Laceration of the blood vessels has been known to follow severe muscular 
exertion. When brisement force for the treatment of ankyloses of the knee 
joint, occasioned vessel rupture, gangrene of the extremity was a complica¬ 
tion in 9 cases (Salzer 1 ). 

Gangrene of the lower extremities is a complication of severe general body 
concussion and after burial or entombment under earth following explosive 
shells that have penetrated into nearby earth. The gangrene has often been 
attributed to thrombosis of the vessels. In other cases, where the upper 
extremities were also involved, the cause remained obscure, since the vessels 
were found patent. Perhaps some of these eventualities are referable to a 
traumatic vasomotor spasm (Chap. XCIII). When both artery and con¬ 
tiguous vein are injured, a so-called arterio-venous aneurysm may develop. 

Results of Recent Injury.—Partial injury of the vessel wall with laceration 
of the inner layers, although unattended with hemorrhage, may lead to gan¬ 
grene of the peripheral parts as a result of thrombosis and embolism. 
Usually, however, hemorrhage is the first sign of vessel injury. 

We may distinguish between internal and external hemorrhage depending 
upon whether the blood appears ouside of the body, or not. The blood can 
be extravasated into the tissues which it may destroy by compressive and 
extensive forces, and form a spurious aneurysm. 

The degree of hemorrhage depends upon the size of the vessel, and that 
of the wound. If the blood does not find an exit externally, cessation of hem¬ 
orrhage usually follows by reason of the pressure of the accumulating extrava¬ 
sation; this may occur even without thrombosis. On the other hand, the 
infiltration with blood may continue into the muscles of the thigh and gluteal 
group until exitus occurs. 

Bleeding from the veins is not as dangerous as the arterial, and more easily 
arrested through compression bandages. 

Another immediate sequence of injury to the veins is air embolus. This 
may occur at operation, or especially as the result of bullet or war wounds. 
Where the diagnosis can be made, the symptoms preceding death are pallor, 
slight cyanosis, spasms of the facial muscles, sometimes opisthotonos and 
cessation of respiration. A peculiar murmur through the vein wall is a signi¬ 
ficant sign of the entry of air. 

Thrombus formation in the vessels implicated in war wounds is not as 
common as is supposed, at least as far as larger vessels are concerned. Borst 2 
believes that even larger tears and perforations may occur in vessels without 
thrombus formation. Late thrombosis may occur in parietal or obturating 
fashion, and then is said to bear some relation to secondary infection. As 
pointed out in the Chapter on Thrombosis there is still much discussion as to 
the role of infection in the production of thrombosis. Stich reports extensive 
thrombosis in larger arteries that he exposed because of the fear of secondary 
hemorrhage in cases of bullet wound injuries. 

1 Salzer, Wien. med. Wchnschr., 1884, No. 89. 

2 Borst, in Borchard-Schmieden, Lehrbuch d. Kriegs chirurgie, Barth. Leipzig, 1917. 


206 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Where infection is associated with thrombosis as the result of blood 
vessel injury, rapid extension of the thrombotic process not only in the 
arteries, but in the veins may continue without interruption even into the 
common iliac or inferior vena cava. 1 Where the thrombotic process is not 
sufficiently extensive to cause gangrene, other grave sequelae may occur, 
amongst which may be numerated the following: Recalcitrant edemas, 
severe paresthesiae, and marked functional impairment of the limbs. 

When the circulatory symptoms are of milder degree, the patients com¬ 
plain of a feeling of coldness, formication, and numbness. Compression 
through extravasation of blood may cause symptoms without implication of 
the larger arteries themselves, the hemorrhage ocurring from smaller vessels. 

Spasm of the vasoconstrictors (Chap. XCIII) has also been observed 
following bullet wounds in the neighborhood of large vessels. As an example 
may be cited a case of Kroh. 2 

After an infantry wound of the inguinal region, a soldier complained of numbness and 
formication in the foot. The femoral pulse above the bullet wound was barely perceptible. 
The skin below the knee, inclusive of the toes, was yellowish white, cold, anemic, insensitive 
to touch and to needle pricks up to the region of the upper calf. The pulse on the healthy 
side was strong and full. A diagnosis of vasomotor spasm was made, and massage and 
elevation were ordered. Nine hours later sensibility and pulses had returned to the normal. 

In another case the same author demonstrated at operation that the vascular sheath 
was infiltrated with blood, but not opened. When the femoral artery was exposed, its 
caliber was about that of a knitting needle, but under the observation of the operator it 
gradually returned to normal. 

Complications.—The most frequent complications are nerve injury or 
neuritis, pressure effects upon neighboring nerves or irritative phenomena. 
In view of the proximity of nerves and larger arteries, it is comprehensible 
that sensory disturbances are frequently associated with vessel injuries. The 
proximity of the ulnar and median nerves to the brachial artery accounts for 
the well known combination of vascular and nerve symptomatology. In 
bullet wounds in this region, the following symptom-complex is not uncommon: 
the extremity becomes cold and cyanotic, hyperhidrosis develops, and later 
muscle atrophies and contractures, giving a picture not unlike that of ischemic 
contracture. 3 

Some authors emphasize that actual organic implication of nerves is 
altogether responsible for the vasomotor and contracture symptoms. On the 
other hand, there are data available which suggest that the arterial lesions and 
involvement of the periarterial sympathetic plexuses or nerves may give 
similar clinical pictures (Chap. XCII). 

Severe circulatory disturbances • usually of the upper extremities may 
attend bullet wounds of large arteries and lead to ischemic contracture of the 
muscles, without gangrene. Bier reports a number of cases in the upper 
extremity, usually after injury to the brachial artery. The following example 
may be quoted. 

Bullet wound of the brachial artery of the right arm in a young lieutenant was followed 
by severe contracture of the muscles of the forearm. About 6 years later the following was 
the status: The musculature of the forearm was “stony” hard, and only slight motion was 
possible in the stiff fingers, the wrist joint being ankylosed. The hand was cold, the sensa¬ 
tion undisturbed, except in the ulnar territory, and the elbow joint mobile. The fingers 
were in a position of marked flexion, and discolored bluish red; the peripheral pulses were 
imperceptible. 

1 See discussion of the stagnation thrombi associated with embolism when infection is 
present, Chap. LXXXV. 

2 Kroh, Bruns. Beitr. z. klin. Chir., 1917, 108, 61. 

3 See case of embolism of the brachial artery operated upon by the author, in which such 
symptoms developed, pp. 495, 496. 


INJURIES TO THE BLOOD VESSELS AND GANGRENE 


207 


The lesions of ischemic degeneration following ligation of large or main 
arteries of a member have been described (Leriche and Policard 1 ) as includ¬ 
ing the following: In the marginal zones between regions poorly and ade¬ 
quately supplied with blood (i) an absence of all inflammatory phenomena; 
(2) characteristic changes in the small arteries and arterioles, namely, degen¬ 
eration of the muscular elements of the media with conservation of the 
connective tissue. 

In the ischemic territories the following muscle alterations are worthy 
of emphasis: (1) a rapid degeneration of the muscle fibers that attains a 
certain degree at which the process is held in statu quo over a long period of 
time; (2) segmentation of muscle fibers in discs and the disappearance of 
nuclei; (3) augmentation of the amount of fibrous connective interfibrillar 
and interfascicular tissue, the nuclei here also being lost. 

Injury of a Main Artery or Vein.—Wounds of large arteries give rise to 
symptoms that vary according to whether there is a sufficiently large 
wound to permit of the escape of the blood, or whether infiltration of the 
deeper tissues with the escaping blood takes place, with the formation of a hema¬ 
toma. When one of the chief vessels of an extremity is torn, the peripheral 
portions of the limb, become pale, cold, somewhat insensitive to pain or 
anesthetic. These manifestations may persist, or be evanescent. As a 
rule, the collateral circulation becomes rapidly established, and it is only in 
rare cases that gangrene follows an arterial injury, or wound, when the blood 
can escape externally. However, when the tissues are infiltrated, and a large 
hemorrhagic exudate is formed, gangrene is more frequently the issue. 

Interesting and instructive observations could be made on the results of 
injury of the femoral artery during the Great War. Only in some cases did 
gangrene develop. 

When there is an open wound of the thigh involving the femoral artery or vein , lethal 
bleeding takes place so rapidly that surgical aid rarely, if ever, comes into play. Where 
the entering body is small and takes an oblique course, closure of the external wound may 
take place, and by virtue of deep hemorrhage the collected masses of blood may by great 
pressure, bring about a cessation of the hemorrhage. Small holes in the femoral arteries 
may heal spontaneously or lead to the development of traumatic aneurysm. 

Late or secondary hemorrhages and secondary erosion of the vessel wall may lead to 
grave consequences. 

Symptoms .—The thigh is'enormously swollen and tense. Large hematomata can spread 
in the direction of the scrotum and perineum. Characteristic is the pulsation which when 
it can be elicited over the hematoma, gives the picture of a pulsating hematoma. With this 
there may be absence of the pulse in the dorsalis pedis and posterior tibial, circumstances 
that make a diagnosis of injury of the femoral artery certain. However, the presence of 
pulsation in the vessel does not necessarily indicate an intact femoral artery. Within a few 
days a typical bruit can develop and this may be either systolic or systolic-diastolic, when 
an arteriovenous aneurysm is present. 

Associated with the swelling are severe pain and paresthesiae, due either to injury to the 
nerves themselves or to their implication in the bloody exudate. 

Secondary hemorrhages may take place through the bullet tract, and these are of grave 
import. 

Secondary infection also may give concern, and may occur early within a few days or 
late, even after a week. 

1 Leriche and Policard, Compt. rend. Hebd. de la Soc. de Biol., 1920, p. 415. 


208 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XXXVII 
ANEURYSMS 

Pseudo-aneurysms.—A false aneurysm or pulsating hematoma may result 
from a condition in which an extravasation of blood remains in communica¬ 
tion with an injured artery. Other appellations recently given to this condi¬ 
tion are communicating or pulsating hematoma. By some authors this is 
described as a transitional stage in the development of a traumatic aneurysm, 
for in a few weeks the hematoma may become distinctly demarcated and 
circumscribed against the surrounding healthy tissues, and become converted 
into an aneurysm. 

These pseudo-aneurysms or pulsating hematomata vary in size, depending 
upon the caliber and situation of the injured vessel; also upon the size and the 
form of the vascular wound, the initial treatment given, and the circumstances 
attending the transportation of the patient. Thus, it has been observed 
that relatively small vessels such as the radial artery give rise to hematomata 
that are as large as those of subclavian origin. Pulsating hematomata are 
usually larger in the case of arteries, than when a simultaneous injury of 
artery and vein occurs. 

Nor is there a constancy in the size of the hematoma. After cessation 
of hemorrhage a shrinkage of the mass is observable due to resorption of 
blood; or, by reason of increased pressure after exertion, constipation, or 
other mechanical influences (sneezing, defecation) late hemorrhage into the 
sac may occur with enlargement of the mass. Or, infection of the sac may 
bring about similar changes in volume. 

With the coagulation of the blood a stratified or onion-like deposition of 
coagula takes place in the hematoma with white, red, and mixed thrombi. 
Those masses that are in immediate apposition with the tissues become 
organized first, and constitute the sac of the aneurysm, whereas the more 
centrally situated contents are masses of cruor, blackish, reddish blood of 
varying consistency. It is remarkable that the circulation may continue 
in spite of the communicating thrombotic and cruor masses. Indeed, even 
the peripheral pulses may be conserved. 

Anatomically the pseudo-sac is made up of a thin fibrinous membrane, 
composed of homogeneous fibrin enclosing leukocytes and red blood cor¬ 
puscles. There is no endothelial lining in all of the recent cases. 

Traumatic Aneurysms.—For a comprehension of the circulatory dis¬ 
turbances of the extremities only the salient features of these types of aneu¬ 
rysms and their role in the production of vascular disturbances require 
mention here. Further data with surgical bearing must be sought in the 
surgical literature. 

A traumatic aneurysm is produced by virtue of encapsulation of a pulsat¬ 
ing hematoma. A distinction has been made between false and true aneu¬ 
rysms. The former designation has been applied to aneurysms arising in 
consequence of injuries to a normal vessel wall through dull or sharp force; 
the latter has been referred to circumscribed or circumferential dilatation 
of the vessel. A distinction has been made between two varieties; false 
aneurysms in which there precedes a defect in the wall of the vessel, and true 
aneurysms that are still lined with an attenuated and dilated wall. Some 
authors would extend the term, aneurysm, so as to include all dilatations 


TREATMENT OF INJURIES TO THE BLOOD VESSELS 


209 


irrespective of whether they develop spontaneously or after traumatic 
lacerations. 

The terms diffuse false aneurysm and circumscribed false aneurysm are found in the 
literature descriptive of recent arterial injuries on the one hand, and older encapsulated 
products on the other hand. Another appellative, encapsulated hematoma, either pulsat¬ 
ing or non-pulsating has been suggested (Schum). 

Symptoms.—Only those features concern us here that relate to the circu¬ 
latory disturbances occasioned in the affected extremity. Referring briefly 
to the general symptomatology, this may be summarized as follows: first, 
tumor formation brought about by the presence of one or more partly or 
completely organized blood sacs arising from the vessel; second, a pulsation 
of this sac synchronous with the arterial pulse 5 third, a murmur synchronous 
with the cardiac systole; fourth, circulatory disturbances in the peripheral 
course of the artery and its branches with changes in the peripheral pulses; 
fifth, manifestations due to implications of accompanying nerves (irritative 
phenomena of the sensory fibers, paraesthesia pain, paralytic symptoms) 
with involvement of either motor or sensory fibers; and sixth, contractures 
implicating neighboring joints. 

We shall dwell only upon those circulatory and neurogenic disturbances 
that are germane to the subject matter in hand here. 

Circulatory Symptoms .—The peripheral pulse may be felt beyond the site 
of the aneurysm, or may be absent due to complete occlusion of the artery, 
because of compression of the.artery by a sac against non-yielding supports, 
such as bone; or due to kinking of the arterial channel from overdistension 
of the sac and the direction of its growth. When a pulse is present, it may be 
diminished as compared with the healthy side. 

Complications and Gangrene.—The most important’of these is hemorrhage 
which can occur externally or into the tissues, particularly in traumatic 
aneurysms. Late secondary hemorrhage is not uncommon and a not in¬ 
frequent cause of a lethal outcome. Indeed, it may occur from the first to the 
fifth week, or after 2 months. 

The symptoms of internal bleeding are the following: increasing pain in 
the extremity, paraesthesia, swelling edema. As the result of the compressing 
action of the hematoma, ischemic contractures, disturbances in the nutrition 
of the whole extremity, and even gangrene may occur. 


CHAPTER XXXVIII 

TREATMENT OF INJURIES TO THE BLOOD VESSELS 

In recent injuries of the blood vessels, our aim should be a two-fold one; 
firstly, the prevention of the immediate danger of the loss of blood;and 
secondly, the restoration of the circulation of the part. 

The Control of Hemorrhage.—Little emphasis need be laid upon the 
value of the Esmarch rubber tourniquet, for the prevention of hemorrhage 
from an extremity. Occasionally, it is well to sew up a wound tightly when 
bleeding occurs from regions inaccessible to an Esmarch or Martin bandage, 
particularly on the battle field, when complete surgical equipment may not 
be at hand. If the wound be too large, it may be tamponed very tightly and 
the skin sutured over it, a pressure bandage being placed over the whole. 

14 


210 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


These are but temporary measures, and must give way to the permanent or 
final control of the bleeding through other means. 

Another method often suggested is the application of sterile gauze over 
which compression is exerted through a solid unopened well rolled muslin 
bandage. This is made to obliterate the arterial lumen through a compress¬ 
ing force brought into play by a firmly applied superimposed rubber bandage. 
Or, we may be constrained to leave artery forceps in the wound, under 
certain circumstances on the battle field. 

The Permanent Control of Hemorrhage. —The question whether a ligature 
or suture of the vessel is indicated depends upon the size of the vessel, the 
condition of the wound, the circumstances under which hemorrhage must be 
controlled and the presence or absence of adequate surgical material and 
equipment. During the Great War even some of the smaller arteries were 
successfully sutured, when a lateral opening was present (radial artery, Stich). 
Whenever we believe that the ligation of a vessel of moderate size will not 
compromise the integrity of the peripheral parts, ligation may be carried out. 

Given the proper circumstances, an absence of general or local infection, 
and a patient who is in a condition for suture operation, the question of ade¬ 
quacy of collateral circulation is an important one in determining whether 
suture or ligature operation should be attempted. 

For the investigation of the adequacy of collateral circulation a number of 
tests have been employed, particularly the Mosckowicz test (Chap. XXIX). 
This test may be carried out in the following modified manner. 

Taking an injury of the femoral artery as an example, the limb is made ischemic either 
through elevation, or better still, through the application of a rubber bandage, below the 
point of injury. Thereupon the femoral artery is compressed against the pubic bone until 
all pulsation below disappears. The rubber bandage is taken off after about 2 minutes, 
and the limb either kept at the horizontal or preferably depressed. If the collaterals are 
adequate, a hyperemic reaction takes place up to the tips of the toes in spite of the continued 
compression of the femoral artery. It must be remembered that it is good to control this 
test by a similar one on the healthy extremity, and that the findings are only reliable if we 
are certain that the artery is being properly obliterated by pressure above. The Lexer- 
Coenen test (Chap. XXIX) also described by Henle and others may give valuable infor¬ 
mation if it is positive, and the rapid almost pulsating arterial flow from the arterial stump 
gives evidence of sufficient collateral circulation. 


The Relation of Larger Arteries to Nutrition of the Part. —The effects of 
ligation of the femoral artery have been variously estimated. According to 
Wolff (1908) the following percentages were given for various larger arteries, 
as to the incidence of gangrene of the lower extremity after ligation of 
various large arteries. After ligation of the external iliac 50 per cent gangrene; 
common femoral both above the profunda 25 per cent; popliteal 40.9 per cent; 
femoral below the profunda 12.7 per cent. As for the upper extremities, 
gangrene was noticed after ligation of the axillary artery in 15 per cent; sub¬ 
clavian and brachial about 4.8 per cent. 

Treves had already pointed out, years ago, the great risk attending liga¬ 
tion of the common femoral artery. Observations during the late war, 
however (Sencert) seem to indicate that ligature of the femoral artery is not 
as dangerous to the vitality of the limb as is commonly believed. This 
author ligated the femoral 11 times (in 3 the common femoral) with no case 
of gangrene. Only where there was a large hematoma did gangrene occur 
(9 examples of the latter). 

Heidrick reports that gangrene follows ligation of the femoral in 20.7 per 
cent of the cases. This author is in accord with the view already expressed 


TREATMENT OF INJURIES TO THE BLOOD VESSELS 


211 


that gangrene is more frequent following ligation below the origin of the 
profunda than above. 

It is important to take into consideration in any interpretation of the 
consequences of ligation and injury as to the presence or absence of previous 
arterial disease. Infection, trauma, secondary thrombosis all play a role in 
determining whether gangrene will take place or not. 

It must be further remembered that while the skin may be adequately 
nourished after ligation of a large vessel, this does not necessarily pertain 
to the subsequent condition of the deeper tisssues. It is well known that 
the musculature is much more susceptible to diminished blood supply than 
the skin. Therefore, necrosis may take place after ligation, but leave the 
integument intact. In this way can be explained the sequelae after ligation, 
and complications that may occur weeks after the operation. Even ischemic 
contractures have been reported. 

Principles Underlying Surgical Treatment.—For details reference must 
be made to surgical treatises and to the literature in this domain. Certain 
basic facts and observations, however, that are relevant for an understanding 
of the circulatory phenomena and conditions in the extremities merely need 
be dwelt upon here. 

It is now believed that ligation should be made at the point of injury, 
and that both vessel stumps should be cared for. The older admonition 
to treat and ligate the vessel at the site of predilection is fallacious advice, 
since it can neither assure one against secondary hemorrhage, nor is it free 
from the danger of gangrene. Only when the bleeding vessels cannot be 
found nor sought for in view of the local condition of the wound, is the more 
remote or indirect ligation permissible. 

Ligation is only reliable in healthy tissue, so that it may be necessary to 
dissect the artery for some distance, isolate it and tie in more healthy territory. 

Ligation and Treatment of Aneurysms.—If a pulse beyond the aneurysm 
is present, one can defer operation, while if the pulse is absent, extirpation 
can be carried out without any fear of gangrene. 

Experience in the late war has taught us considerable regarding the time 
necessary for the development of collateral circulation. Some authors 
suggest waiting for several months, while others believe that in a period from 
3 to 6 weeks adequate collateral circulation will have become established, 
so that ligation of the artery can be done without danger. Early operation 
after rupture of a blood vessel or formation of a traumatic aneurysm may be 
dangerous, not only because of the absence of collateral supply, but also 
because of the compressing effects of the hematoma, which may be expected 
to become absorbed after sufficient delay. The danger to collaterals is thus 
automatically and gradually removed. 

Whenever ligation of an artery or extirpation of an aneurysm is done, it 
is important to inspect the more peripheral parts of the extremity, as regards 
the circulation, and to obtain a knowledge regarding the condition of the 
collaterals. If the extremity is of good color after temporary compression 
of the afferent artery (leading into an aneurysm) ligation can be carried 
out without fear. If there is doubt, some authors advise small incision into 
the periphery of the extremity, so as to determine whether bright blood, dark 
blood or none is evacuated. If after from io to 15 minutes of observation, 
the extremity is still pale, or has a marmorated appearance, then we can 
conclude that the collateral circulation is inadequate. 

Furthermore, the data furnished by the Henle-Coenen collateral sign 
(Chap. XXIX) are of importance. Considerable discussion has arisen as 


212 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


to the advisability of simultaneous ligation of the accompanying large vein, 
when a large artery is ligated. In the case of arteriovenous aneurysms, this 
matter requires no special decision. When suture is possible, both may be 
conserved; if not, and extirpation has to be done, both have to be ligated. 
When the vein, however, is intact, certain data on observations during the 
Great War would point to the advisability of ligating the vein. 

Thus Wolff 1 reports that after ligation of the femoral artery alone, there 
were 20.7 per cent cases of gangrene, while if the vein also were ligated, only 
8 per cent. In the case of the upper extremities, ligation of the arteries 7.8 
per cent, ligation of both artery and vein—no cases of gangrene. Many 
theories have been propounded regarding the explanation for this pheno¬ 
menon. According to some, a disproportion between collateral afferent 
supply and venous outflow is avoided by ligation of the vein. J ohannessen 2 
published a case in which the lower extremities evidenced very poor circula¬ 
tion after ligation of the femoral, edema and pain. After the vein was 
ligated, 8 days subsequently, a continued improvement in circulation 

° CC Onthe other hand, deleterious consequences have followed ligation of the 
femoral vein. According to the statistics of Braun, 3 the ligation of the 
femoral vein alone, above the profunda produced gangrene in 2.8 per cent of 

Indeed, some authors advise against ligation of the femoral vein, because 
of the likelihood of stasis. On the whole, although there are dissenting 
voices, the majority of surgeons rather favor the simultaneous ligation of the 
artery’ and the vein, with certain exceptions in the case of the lower 
extremities. It is well in each and every case to decide this at the time of 
operation, when by temporary arrest of the circulation of the vein, observa¬ 
tions can be easily made as to whether the circulation is objectively improved 
thereby. 


Neurovascular Syndromes after Ligation of Large Arteries. —There is a clinical complex 
that either temporarily or permanently restricts the muscular activities, when impairment 
of the circulation of a limb follows ligation of one of the larger arteries. It is not surprising 
that a diagnosis of malingering is often made, for, while under the observation of the 
physician little is objectively in evidence. However, upon increased activity and work, 
especially if the latter is excessive, and also under exposure to cold and moisture, circulatory 
disturbances appear. These are coldness and blueness of the hands and feet, reduction in 
the size of the pulses, rapidly developing edema, a sensation of numbness in the extremities, 
and occasionally dull pain. When the limb is put at rest, both objective and subjective 

manifestations appear. .. , , , 

It would seem, in light of experiences during the Great War, that reestablishment of the 
circulation through suture of the artery involved would prevent the development of these 
clinical syndromes. The favorable results obtained by von Haberer with arteriorrhaphy, 
as compared with ligation, definitely demonstrated the advantages of the suture method. 


Arteriorrhaphy.— Opinions are not in accord as to the value of vessel 
suture after injury, some tending to the extreme that the method has little 
or no useful sphere of application, while the other schools employ it even in the 
presence of infection. It appears to the author that arteriorrhaphy, when 
carried out by those sufficiently skilled and with careful technic, is an exceed¬ 
ingly useful procedure that will receive more and more recognition, as the 
experience of the surgeons in this work increases. 

1 Wolff, Brun’s Beitr. z. klin. Chir., 58, 762. 

2 Johannessen, Zentralbl. f. Chir., 45, 516. 

3 Braun, Arch. f. klin. Chir., 28. 


THRtyM BO-ANGIITIS OBLITERANS—INTRODUCTION 213 


The procedure is to be entertained in view of the following dangers of 
ligation; firstly, th^ vascular and neurovascular remote consequences; and 
secondly, the dangers of gangrene. 

Certain authors report successes even in infected tissues, so that the 
view oit accepted that scrupulously clean fields are essential, may have to 
be rejected. 



Among such instances niay be mentioned the case of Danielsen 1 of suture of the axillary 
artery in infected tissues. V. Haberer 2 described 7 cases of arterial suture with healing in 
the presence of severe local infection; and Schoene 3 closed a longitudinal slit in the popliteal 
artery in the presence of a gas phlegmon, with a pulsating posterior tibial artery (!) as a 
result. 

The danger of gangrene consequent upon suture is less than that follow¬ 
ing ligation. The immediate reestablishment of circulation, however, after 
suture does not preclude the possibility of late gangrene. Such has been 
reported as taking place 2, 3 or 6 weeks after the operation, usually gradually 
but in some instances suddenly. In such cases the outcome is due 
to secondary thrombosis. 

The mild circulatory disturbances that are most apt to occur after impaired 
circulation due to arterial injury and ligation are less frequently observed 
after suture, or in much milder form. These disturbances are the following: 
a feeling of coldness, sometimes paresthesiae, sensations of heaviness, numb¬ 
ness and formication. In some patients pain occurs after bodily exertion, or 
a hard edema of the affected limb may ensue. It is the opinion of v. Haberer 
and Stich that objective and subjective disturbances are usually absent in 
those cases of arteriorrhaphy where the peripheral pulses were reestablished 
after the operation. It has already been pointed out that peripheral pulses 
may return weeks after arteriorrhaphy, due to the intervention of collaterals, 
so that only the immediate restoration of the pulses can be regarded as an 
evidence of a successful reestablishment of the arterial paths. 


CHAPTER XXXIX 

THROMBO-ANGIITIS OBLITERANS—INTRODUCTION 


It seems strange that a primarily scientific study of the lesions of thrombo¬ 
angiitis . obliterans—later supplemented by clinical observations—should 
have laid the foundation for a correct appreciation and classification of a 
large number of affections involving the circulation of the extremities. 
Indeed a careful consideration and investigation of all the basic anatomical 
changes as well as the many clinical phenomena characteristic of thrombo¬ 
angiitis obliterans, will do more in a practical way to fashion and shape our 
concepts of the vasomotor and trophic neuroses and all allied organic affections 
of the vessels of the limbs, than the study of any other single or group of 
such diseases. And this is true because manifestations of almost all of the 
morbid conditions in question are represented in this one interesting malady. 

The medical student as well as the practitioner whose diagnostic apprecia¬ 
tion of Raynaud’s disease, erythromelalgia, chronic acrocyanosis, athero- 


' 1 Danielsen, Deutsch. Ztschr. f. Chir., No. 11, 40, 381. 

2 v. Haberer, Arch. f. klin. Chir., 108, H 4. 

3 Schoene, Deutsch. Ztschr. f. Chir., 1918, 143, 84. 


214 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


sclerotic vascular lesions, and thrombo-angiitis may still be obscure in spite 
of reading of text books or of clinical experience, will find his doubts and 
clinical obscurities remarkably clarified by an intensive study of the varied 
manifestations and lesions of thrombo-angiitis obliterans. It is for this 
reason, that the author has deemed it wise to indulge in a comprehensive dis¬ 
cussion of its pathology, its latent and active symptoms. 


CHAPTER XL 

4 

THROMBO-ANGIITIS OBLITERANS—GENERAL CLINICAL 

CONCEPT 

Thrombo-angiitis obliterans 1 is a clinical and pathological entity which 
has been, and is still, incorrectly called “endarteritis obliterans” by many 
authors. The names, presenile, and juvenile gangrene have also been applied 
to it. 

At the onset, thrombo-angiitis obliterans is essentially an inflammatory 
process, involving particularly the deeply situated and larger arteries and 
veins of the lower and upper extremities. Almost immediately after the 
inception of the lesion, there follows extensive occlusive thrombosis, that sub¬ 
sequently gives way to a stage of healing or organization, the final result 
being the complete closure of arteries and veins over a large extent of their 
course by vascularized and canalized connective tissue. Although no 
extensive study has been made of thrombo-angiitis in the vascular domain 
outside of the extremities, the typical lesions have been observed by the 
author: in the spermatic vessels, and according to Murphy, are said to occur 
in the renal vessels. 

Characteristic is the involvement of the superficial veins, of the lower and 
upper extremities in the form of a migrating or thrombo-phlebitis in about 20 to 
25 per cent of the cases. It is in this territory that the most thorough and 
reliable investigations on pathology can be made, as the lesions in the vessels 
then become accessible at the very onset of the malady before the effects of 
organization and healing have confused the histological picture. 

Clinical and Pathological Concept of Thrombo-angiitis. —The disease 
manifests itself in most instances with indefinite pains in the sole of one foot 
(usually the left) in the ankle, or in the toes, the patients being soon disturbed 
in their walk by these symptoms, or by the sudden onset of cramp-like sensa¬ 
tions in the calf or elsewhere in the leg (intermittent claudication). These feel¬ 
ings make the patients take frequent rests, often inducing them to investigate 
the condition of their limbs. Some take off their shoes and rub the part in the 
hope of dispelling the pains or banishing the uncomfortable numbness of the 
toes and feet; others say that the feet become cold and numb when the tem¬ 
perature is low and the weather is inclement. After the lapse of weeks, 
months or even years, evidences of trophic disturbances make their appearance. 
Following the cutting of a nail, or without apparent cause, an abraded spot 
or hemorrhagic bleb, a pustule^or a dry, dead patch of skin develops near the 

1 This name was suggested in 1908 by the author for this interesting and remarkable 
disease and has been almost universally accepted in the United States. 


THROAf BO-ANGIITIS OB LI TERA NS—GENERA L CLINICAL CONCEPT 215 


tip of one of the toes or under a nail. Now the local pain becomes excruci¬ 
ating during the night as well as day, so that some of the sufferers beg foj^ 
amputation of the affected part. 

It is usually during the first attack of trophic disorder, but sometimes 
when only intermittent claudication is present, that the physician or patient 
notices another characteristic symptom, namely, a peculiar blush of the 
toes and forepart of the foot, sometimes extending to the ankle or slightly above, 
when the limb is in a pendent position (Plate IV). Upon allowing the limb 
to hang down, the affected toe soon turns color. It assumes a bright red 
hue which is seen to pass to the other toes and then up the back of the foot 



Fig. 46.—Trophic lesions in thrombo-angiitis obliterans. 

for a variable distance. This reddening is often termed rubor , or may be 
called erythromelia. The elevated extremity on the contrary, rapidly 
becomes blanched (ischemia). Sometimes the superficial ulcer will heal under 
conservative treatment and the patient will either recover perfectly or his 
symptoms will become chronic. At this period his limb may show the trophic 
lesions and scars left by previous ulcers (Fig. 46). The dorsalis pedis and the 
posterior tibial arteries usually fail to pulsate, and ischemia in the elevated 
position and redness of “erythromelia” in the pendent position are regularly 


216 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


elicited. Sooner or later, however, a patch of gangrene develops, the local 
pain becomes intense, and amputation will be the issue. 

Because of the striking condition of redness in the dependent position, 
and because of the increase of local pain when the limb is hanging down, a 
number of clinicians have been accustomed to diagnosticate “erythrome- 
lalgia” in these patients. Some cases have been regarded as examples of 
Raynaud’s disease, because in them the symptoms of blanching and cyanosis 
of the parts were prominent features. Although resembling erythromelalgia 
and Raynaud’s disease in a number of symptoms, the clinical picture of 
thrombo-angiitis obliterans is so characteristic and definite, and the patho¬ 
logical lesions so typical in this disease, that it constitutes a distinct clinical 
entity. 

A general concept of the disease could be briefly formulated in the follow¬ 
ing terms. Imagine a patient seeking relief for acutely swollen superficial 
veins of the lower or upper extremities, of sudden advent, and with all the 
manifestations of an acute thrombo-phlebitis. Imagine this process involving 
a considerable portion of the distal territory of the internal saphenous vein, 
followed by abatement of symptoms, and consequent resolution or healing. 
You will be in no doubt as to the general pathology nor as to the clinical 
course of the condition, though your estimation of the etiology will in most 
instances, at least be obscure. 

Transfer this picture to the deeper vascular system, over the distribution 
of the external and internal plantar arteries and veins, the dorsalis pedis, 
anterior tibial, posterior tibial and the perineal arteries and veins, that is, 
with lesions in territories where objective manifestations are absent—and 
you will be depicting to yourself, what corresponds to our own conception of 
the pathological process in the disease, thrombo-angiitis obliterans. So 
here, too, we postulate, an acute inflammatory and thrombotic lesion, but one 
involving deep arteries or veins, or both, as the initial stage of the pathological 
anatomy. 

Whereas, the patient afflicted with an inflammatory and thrombotic 
lesion of the superficial veins presents objective signs easy of recognition, the 
patient suffering from thrombo-angiitis obliterans in its earlier stages may 
offer no objective evidences suggestive of the true nature, or of the site of the 
lesion. It is but in a very few cases that one is justified in ascribing certain 
symptoms to the incipient stage of the disease. Severe, non-localizable 
shooting pains in the calf or foot, attended with difficulty in walking, or, 
possibly with tender calf muscles, with or without vasomotor symptoms and 
coldness in the foot, with or without obliteration of the dorsalis pedis and 
posterior tibial pulses, may be the only symptoms. It is only when we com¬ 
pare the history with the future clinical course and pathology that we can 
relegate such indefinite signs to the onset of the affection. In most instances, 
however, the patient will not seek advice for such initial symptoms, either 
because they are not sufficiently severe to require the attention of a physician, 
or because they are incorrectly regarded as rheumatic in origin, possibly due 
to trauma, cold, the presence of flat or weak foot, or because they are 
explained on the basis of some other minor ailment. 

S Strange to say, patients afflicted with thrombo-angiitis obliterans may 
present symptoms which differ in no way from those attending the thrombo¬ 
phlebitis of the superficial veins, or so-called migrating phlebitis. These are 
the cases of thrombo-angiitis obliterans in which an acute inflammatory 
thrombosis involves smaller or larger? portions of the external or internal 
saphenous veiiy'radial, ulnar, median cephalic or median basilic vein. Such 

i 


PLATE IV 


Erythromelia 



Rubor in Thrombo angiitis Obliterans. (Buerger ii 
“Surgery,” Vol. IV.) 


Ochsner’s 




THROMB0-ANGIITIS OBLITERANS—GENERAL CLINICAL CONCEPT 217 


cases are the most instructive of all, for they are the ones which afford us 
material for pathological study. Here the veins are accessible; portions can 
be surgically removed when the lesions are in the acute inflammatory stage 
and submitted to histological examination. 

While the former type of cases is difficult to diagnose, the variety with 
concomitant migrating phlebitis can be recognized by a study of the vein 
lesions under the microscope. If the tissue be examined when the lesions are 
still in the early inflammatory stage, before organization or healing has taken 
place, certain characteristic and specific lesions can be identified, changes 
which shall elsewhere be described as pathognomonic for thrombo-angiitis 
obliterans. 

Having learned that the incipient lesion of thrombo-angiitis obliterans is 
an acute inflammatory one, involving the arterial and venous walls, we will 
expect an occlusive thrombosis as the immediate sequence, and will not be 
surprised to find that this stage gradually gives way to one of organization 
and canalization, resulting in a healed product in which the vessel becomes 
converted into a cord, more or less adherent to its surroundings, and in which 
even the neighboring nerves may become agglutinated and enveloped in a 
fibrotic vascular cord. 

It is the interference with the circulatory conditions of the limbs brought 
about by the extensive occlusive process that is responsible for most of the 
clinical manifestations of thrombo-angiitis obliterans. So that it may be 
correctly said that patients afflicted with thromb-angiitis obliterans do not 
usually suffer directly from the disease itself but from the disastrous occlusive 
thrombosis which signalizes Nature’s method of healing a vascular lesion that 
has long since disappeared. 

From a study of the pathological material, and from a comparison of the 
lesion with the clinical history, we must conclude that insidious or clinically 
unrecognizable exacerbations of the lesion may occur from time to time, so 
that the involvement of the vascular territory with the obliterative lesion is 
a progressive one until the summit of the organized clot reaches the popliteal, 
in rare cases the femoral or even the iliac arteries. It will not occasion 
astonishment, therefore, that clinical manifestations, too, become more and 
more serious as time goes on. 

Nor must we be surprised if thrombo-angiitis obliterans simulates clinical 
complexes brought about by arterial occlusion from other causes. Differen¬ 
tiation from arteriosclerosis, endarteritic occlusion, and other thrombotic 
conditions may at times be difficult. It is the fact that thrombo-angiitis 
obliterans occur in very young individuals in whom both the vis-a-tergo and 
the cardiac power are adequate for compensation, and in whom the vascular 
adaptability is elastic in its scope—it is this fact that accounts for the seem¬ 
ingly almost inexplicable circumstance that gangrene occurs so late, or may 
be absent, in spite of vast and extensive obliteration of arteries and veins. 
It is to the development of the collateral circulation, therefore, that we owe, 
in part at least, the production of a very peculiar, striking, and characteristic 
clinical picture, recognizable even though manifestations of the acute stage 
of the disease, or manifestations, such as migrating phlebitis are absent. 


218 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XLI 

THROMBO-ANGIITIS OBLITERANS—ACUTE STAGE 


More interesting than the study of the usual manifestations, due to 
impaired circulation, is the investigation of those phenomena that are clin¬ 
ically referable to the “acute stage,” that correspond to the acute inflamma¬ 
tory invasion of the deep arteries and veins. As elsewhere pointed out, 
when the patient seeks advice, he no longer suffers from the affection thrombo¬ 
angiitis per se, but from the “healed stage” (in the pathological anatomical 
sense) where the vessels have discarded their inflammatory products, have 
become converted into hard fibrous cords, and are only in so far responsible 
for the clinical picture, in that their function as conductors or vascular chan¬ 
nels is completely in abeyance, the symptoms being altogether due to a lack 
of circulation” or a mechanical interference with the delivery of blood. A 
diligent search for manifestations attributable to the attacks of deep thrombo¬ 
angiitis or thrombo-phlebitis may find its reward in the discovery of treatment 
or prophylaxis, available and applicable before extensive closure of vascular 
channels has taken place. Such is the importance , then, of the recognition of 
signs that may be interpreted as coincidental with the onset of acute lesions. 

The Acute Symptoms. —These, as far as the author has been able 
to detect, are lancinating pains in the legs, especially in the calf, and foot, 
cramp-like pains in the leg first interfering with walking, later requiring com¬ 
plete rest, tenderness in the calf and along the anterior tibial region, simul¬ 
taneously with, preceded by or unassociated with attacks of migrating 
phlebitis. These manifestations may last for a variable time, are 
unattended with trophic disorders, but accompanied by development of ische¬ 
mia on elevation without or with evidences of disappearing pulsey' When 
the closure of the vessels is confined to the peroneal, and distal vessels such 
as the plantar and peripheral distribution of the anterior tibial artery, and 
even when a portion of the anterior tibial high up is involved, the posterior 
tibial in its usual situation behind the malleolus and the dorsalis pedis may 


& 


be found pulsating. 

The suddenness of the onset of pain in both legs with the absence of true 
intermittent claudication at the incipiency of the trouble, with the slow 
appearance of the usual signs, justifies the assumption that a period due to 
“acute involvement of the deep vessels” was here exemplified in the clinical 
examples at hand. Observed carefully from the stage where none of the 
objective signs of thrombo-angiitis obliterans were associated with attacks of 
pain in the calf and leg, up to the time when distinct manifestations could be 
recognized, the following case permitted of the clinical separation into first a 
stage of acute thrombo-angiitis obliterans, with symptoms referable to the 
disease per se, and a second stage that of symptoms due to arterial obturation, 
a period usually regarded as representative of the disease itself. (Cicatricial 
stage; stage of mechanical hydrostatic and then trophic disorders.) 


N. S., male, Russian Hebrew, age 26, August 28, 1916, began eighteen weeks ago with 
sudden severe cramp-like pain in the calf of the left leg radiating upward into the thigh. 
This was treated as sciatica in one of the hospitals without improvement. Soon thereafter 
a similar attack occurred in the right leg which made walking difficult. There were no 
external noticeable changes to account for the trouble. Physical examination revealed no 
ischemia, no rubor, none of the signs of thrombo-angiitis obliterans, other than doubtful 
pulsation in the dorsalis pedes arteries. 


THROMBO-ANGIITIS OBLITERANS—CHRONIC STAGE 


219 


December n, 1916 (about three months of continued difficulty in walking) in the region 
of the left calf, along the course of the peroneal and posterior tibial arteries, there was 
marked tenderness; no change in the pulsations but ischemia now marked; so also reactionary 
rubor with rather distinct cyanosis in the pendent position. 

January 2, 1917. Now there is no doubt as to the absence of the dorsalis pedis in the 
left leg. In short, first a stage of pain without further symptoms; second the development 
of tenderness in the calf corresponding to the course of the vessels with some cyanosis in the 
pendent position, and third, the development of ischemia , reactionary erythromelia and 
pulseless dorsalis pedis artery. 

Although in the main, it is a difficult matter to recognize the symptoms 
that are referable to the acute process in the deep vessels, certain symptoms 
have been noted in a number of cases, that were sufficiently suggestive to 
warrant being interpreted as due*to the deep thrombosis and inflammation. 

M. P. gave a previous history of migrating phlebitis for which he was admitted to the 
Mt. Sinai Hospital. On May 24, 1908, a physical examination was made by the author. 
He had been in the hospital once before, on August 15,1907, for phlebitis migrans. He was 
again suffering from an attack of phlebitis now involving the saphenous vein and its tribu¬ 
taries to the middle of the left leg, and also the ulnar vein near the left wrist. Now for four 
days he had had paroxysmal attacks of deep pain in the right leg especially in the region of the 
calf, not attributable to the superficial parts. Neither the dorsalis pedis nor the posterior 
tibial arterv could be felt pulsating. These attacks were carefully observed. There was 
no apparent cause for them; and it is more than likely that they were due to inflammatory 
thromboses of the deep vessels, similar to those involving the superficial veins. The 
gradual development of erythromelia and moderate ischemia in the elevated position, were 
corroborative signs. Although the pain had disappeared after four days, the rubor 
persisted. 

The future course confirmed the suspicion of involvement of the deep vessels, since in 
1909 trophic disturbances of both feet developed, and amputation of the right leg became 
necessary; in 1911 the left leg was also lost through amputation. 



CHAPTER XLII 


THROMBO-ANGIITIS OBLITERANS—CHRONIC STAGE 

It is only through a knowledge of the vicissitudinous paths followed by 
the sufferer with this disease in his quest for a cure, and by a study of the 
diversity of combinations that the usual manifestations may present, that a 
comprehensive understanding of the mutations in the pathological process 
and of the prognosis can be obtained. But a relatively few of the manifold 
types will be mentioned here; the affection as it is associated with migrating 
phlebitis (Chap. LVIII) and as it involves the upper extremities (Chap. LIX). 

1. Cases without Trophic Lesions or Gangrene. —By these, we mean that 
certain patients exhibit merely the usual subjective and objective manifes¬ 
tations of impoverished circulation over years of clinical observations (2—10 
yrs. or more), but may at any time thereafter be afflicted with ulcers or a 
mortifying process. For years, with or without attacks of migrating phle¬ 
bitis and intermittent claudication, chronic rubor develops, the foot is 
distinctly blanched on elevation, the dorsalis pedis and posterior tibial 
pulses are absent (sometimes the popliteal) but trophic disorders do not 
appear. 

2. Cases of Exquisite Chronic Rubor , with dystrophic changes, loss of 
merely one or more phalanges after 16 or more years of suffering (case D. B.), 



220 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


deceive the prognostications of the clinician. After prodromal phlebitis of 
either upper or lower extremities recurring for years, coldness, cyanosis an 
pain with chronic rubor develop, so that a painful limp is established, a 
phalanx or more may be lost, but the limb, except for slight edema, puffy 
toes and angry red color, appears intact. This picture is analogous to that of 
chronic pseudophthisis or chronic (vascular) atrophy with rubor described as 
characteristic of arteriosclerotic vascular occlusion. In the former however, 
the age of the patient, the migrating phlebitis, the puffy toes the swollen 
rather than withered foot, are distinctive differential points (case D. B. 

Chap.LVIII, p. 287). , . , 1 , 

* Trophic Lesions the First Symptom. —As shall be pointed out elsewhere, 
the disease may be present in a latent form in either or in both lower extremi¬ 
ties so that it may happen that the patient believes himself well until a 
blister appears (big toe in case D. K.), the toe and foot become red and pain¬ 
ful. Objectively, erythromelia is marked, the usual pulseless vessels are 
demonstrable, a trophic ulcer has developed, and gangrene is imminent. 

4. Cases of Short Duration (Acute and Subacute)— Although the usual 
course of the disease is a chronic progressive one with a long prodromal period, 
then the gradual development of trophic disorders and finally gangrene, there 
are cases in which very rapid development of gangrene can take place, it is 
barely possible that the initial symptoms are not noticed, their development 
being insidious and too slight to warrant attention. Thus. 

M. G., 35 years of age, Russian Jew, apparently well until four months before examina¬ 
tion (June 30, 1009), noticed coldness of the left foot and then pain in the toes which rapidly 
became so severe that it was necessary after some two months to go to bed. Now, four 
months after the onset of the disease, the big toe of the left foot has become black, and the 
tips of the fourth and fifth toes are also becoming mortified At the time of examination 
there were distinct evidences of gangrene of the fourth and fifth toes, absence of pulsation 
in the dorsalis pedis and posterior tibial vessels, and the usual signs of thrombo-angutis 
obliterans. Within a few days amputation became necessary. 


In short, within about four months the disease ran a complete course with 

the loss of one limb. . . , . 

5. Sudden Gangrene Simulating the Embolic Type.— Although the develop¬ 
ment of gangrene is usually a slow process passing through the stages of 
superficial necrosis, ulcer formation and then gangrene of one toe at a time, in 
rarer instances after a period of the usual preliminary subjective manifestation, 
upon cutting a nail or apparently without cause, extensive gangrene of several 
or all the toes including the forepart of the foot may develop within a very 
jew days. Such a course would indicate that either a fresh accession of 
thrombosis took place in many arteries with inadequate opportunities for the 
establishment of collateral paths, or that an involvement of the popliteal 
cut off the collaterals upon which the nourishment had previously depended. 
When seen with gangrene well established, the clinical picture is confusing, 
simulating mortification of embolic, thrombotic and arteriosclerotic processes. 

6. Cases without Symptoms. —Very frequently the disease is overlooked by 
the patient in one limb, whilst it is active in the other, or has existed for years in 
one leg, remaining unnoticed until the advent of the more serious and distressing 
manifestations calls his attention to the affection in the other limb. It is not 
uncommon to find on examination of a case presenting the typical objective 
phenomena in one extremity, that the other leg is the seat .of the same disease, 
physical examination revealing signs of extensive arterial obliteration and 
signs of occlusion of many vessels. Other objective phenomena, too, warrant 
the assumption of an insidious onset with subsidence of the acute lesions, and 
the establishment of adequate collaterals. To cite a case: 


THROMBO-ANGIITIS OBLITERANS—CHRONIC STAGE 


221 


M. P., the supposedly healthy leg evidences marked redness of the big toe and adjoining 
region with some ischemia on elevation, and with the appearance of cyanotic patches over 
the tips of the toes. Reactionary erythromelia is pronounced, being a phenomenon never 
seen in a healthy leg. 

The dorsalis pedis, posterior tibial and popliteal arteries are pulseless^-. 

Comparing this type of involvement with that of the other leg in which the objective 
manifestations were more pronounced, we find the following in the latter. First, marked 
erythromelia even in the horizontal position varying in intensity, there being a play of colors 
such as is seen in the vasomotor cases. Alternating rubor with patches of ischemia is seen, 
the red color predominating. Second, the tumefied condition of the foot with the dis¬ 
appearance of the normal irregularities.* Third, the markedly cadaveric appearance on 
elevation. Fourth, the very slow return of color on depressing the foot after previous 
elevation. Fifth, the extreme descent below the horizontal necessary before any color 
returns in the foot (small angle of circulatory sufficiency). 

From this we may conclude: First, that both legs may be intensively 
involved with thrombo-angiitis obliterans, one of them alone giving sub¬ 
jective symptoms; secondly, that extensive obliteration of the vessels as 
manifested by the absence of pulsations in the dorsalis pedis, posterior 
tibial and popliteal arteries may occur without symptoms; and thirdly, that 
certain physical signs, however, can be elicited, which will show that the leg 
which gives marked clinical manifestations and is more recently affected is 
the more profoundly implicated in the vascular occlusion. So also in the 
following patient: 

P. A. had four years of indefinite symptoms of rheumatism and pain in the ankle, worse 
in cold weather. After a trauma of the dorsum of the right foot, an ulcer formed which 
refused to heal. Somewhat later another ulcer appeared near the base of the little toe of 
the same foot. 

Physical examination showed the typical involvement of the right leg,, erythromelia, 
ischemia, absent pulsation of the posterior tibial, popliteal and dorsalis pedis arteries. 

After a period of observation of about one month, edema developed and finally amputa¬ 
tion became necessary, a Gritti being done with a successful result. 

While in the hospital it was also seen that the left leg was involved in the same process , 
although the patient did not know of this, the signs being marked reactionary erythromelia. 
slight ischemia and absence of pulsation in the dorsalis pedis, popliteal and posterior tibial 
arteries. 

7. Cases with Intermittent Claudication Only .—These are the patients 
who are apt to consult the orthopedist and run the gamut of mechanical 
appliances for an affection in which the vessels are at fault. Careful physical 
examination should elicit, in addition to pulseless vessels, some ischemia on 
elevation, either chronic or at least reactionary rubor with other signs. 

Or, closed vessels and intermittent claudication may make up the complex 
for years, but sooner or later ischemia and rubor are apt to develop, and then 
the trophic lesion. As illustrated in one of the cases (I. M.) intermittent 
claudication was the chief symptom for four years, with absent pulsation of 
the dorsalis pedis and posterior tibial of the left leg, without erythromelia 
or ischemia. 

Or, after a period of intermittent claudication, the other phenomena 
appear, many years being required for gangrene to set in. 

M. L., aged 32, Russian Hebrew, examined on December 12, 1914. After about one 
year of intermittent claudication the left leg showed marked redness, ischemia on elevation, 
absence of dorsalis pedis, posterior tibial and popliteal pulsations, without any trophic 
disorders. At the same time, the right leg was also involved, the main symptoms being 
coldness of the big toe, cyanosis, absence of the dorsalis pedis and posterior tibial pulsations 
without any other symptoms. 

8. Cases with Intermittent Claudication and Migrating Phlebitis Only. - 
Here the patient consults us for the pain on walking, the phlebitis not being 
complained of, but a history of such is elicited on questioning. 


222 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


D., January 29, 1915, aged 20, Russian Hebrew, began five years previously with pain 
in the right calf and sole on walking. One year later he had migrating phlebitis along the 
inner side of the right thigh; none since. For six months the left foot has been affected 
with intermittent claudication, but not so severely as the right. No migrating phlebitis in 
the left leg, no history of trophic disturbance. 

Physical examination. In the horizontal position both feet look fairly normal; no 
further evidence of phlebitis. Both femorals pulsate, the left posterior tibial pulsates, the 
right does not. The right dorsalis pedis is absent, the left present. In the pendent posi¬ 
tion erythromelia appears slowly but with moderate intensity over the whole of the right 
foot and lower leg. No evidences of trophic disorder. In this position the blanching comes 
on rapidly over the toes and the dorsum of the left foot. The ischemia in the left foot, 
however, is only moderate, for, on pressure it is seen that some blood reaches the toes. On 
elevation, after depression, the toes of the left foot lose the red rapidly, but develop only 
slight ischemia. In the right leg, however, there is more ischemia, but not marked. 

Summary .—This is a case in which the right limb alone was affected, 
the symptom of intermittent claudication dominating, migrating phlebitis 
having been present. After four years there was subjectively only inter¬ 
mittent claudication, objectively, marked erythromelia, absent dorsalis 
pedis, posterior tibial, slight ischemia, and no trophic disturbances. Here 
was a very slowly progressing case with only slightly marked symptoms. 

9. Cases Losing the Limb Last Affected .—Not infrequently the leg last 
affected will be the first to require amputation. Among numerous instances 
may be mentioned the following case. 

A. P., with typical symptoms involving the right foot which began in May, 1906, with a 
burning sensation on walking, would frequently have to go into a neighboring park on his 
way home to take off his shoe and investigate the cause of the pain. Then, during the 
winter months came the feeling of coldness and soon a dark bluish black spot developed over 
the base of the fifth toe. Finally, ten months after the onset of the trouble, and after cut¬ 
ting a callus in the painful region, a sore developed which refused to heal. He was admitted 
to the Mt. Sinai Hospital in April, 1907, where it was found that he had a trophic ulcer on 
the outer border of the right foot near the head of the fifth metatarsal bone. There were 
also the usual typical symptoms, ischemia on elevation and rubor in the dependent position, 
the dorsalis pedis and posterior tibial arteries being pulseless. 

In two months, however, the ulcer had healed and from then on the foot gave him no more 
trouble. 

In the meantime, however, the typical symptoms of thrombo-angiitis obliterans devel¬ 
oped in the other leg, leading finally to amputation during the following year. 

Not infrequently the disease exists in one of the limbs for months or years 
without the knowledge of the patient, and is only discovered when symptoms 
referable to the second leg are noticed by him. In such cases the process 
is either developed insidiously or manifests itself simply by the presence of 
intermittent claudication or difficulty in walking, finally coming to a stand¬ 
still without the development of trophic disturbances or gangrene. In the 
meantime the other limb is affected by more severe manifestations, ulcera¬ 
tion and finally gangrene. 

Such a case was J. G., aged 39, Austrian Hebrew who was seen November, 1908. Some 
fifteen years ago he had been troubled with weakness of the legs and thighs on walking 
and standing, also with indefinite pains which were only relieved by rest. These were 
severe enough to incapacitate him for one year. He was apparently well until three months 
ago, when a similar affection involved the right leg and then the foot became noticeably red 
in the dependent position. Soon after an ulcer developed on the dorsum of the right foot 
near the root of the fourth and fifth toes, which healed spontaneously, and then another 
ulcer appeared on the right fifth toe. 

The physical examination in February, 1909, revealed evidences of involvement of both 
legs. The popliteal, dorsalis pedis and posterior tibial pulses of the right leg were absent, 
and on the left the posterior tibial and dorsalis pedis were also negative. The right foot was 
somewhat enlarged, tumefied, all the toes slightly thickened, a patch of gangrene being 
observed on the outer aspect of the fifth toe; marked erythromelia, in the dependent posi¬ 
tion, marked blanching on elevation. The left leg showed intense ischemia on elevation, 


THROMBO-ANGIITIS OBLITERANS—CHRONIC STAGE 223 

and upon depressing the leg after preliminary elevation marked compensatory erythromelia 
most striking over the dorsum was noticed. 

In short, we have here a case in which, except for the history of some 
indefinite pain and intermittent claudication fifteen years previously, nothing 
referable to the left leg could be elicited, although ischemia, erythromelia, 
and absent pulsation were distinct evidences of the presence of the disease 
in this limb. 

On March 25th the right leg was amputated because of gangrene, the left 
leg having in the interim again developed more active symptoms in the form 
of marked redness and pain. 

This was, therefore, a case of insidious development of the disease in one 
leg and its spontaneous cure, the trouble lighting up in the other and lead¬ 
ing to gangrene of the limb. 

10. Cases with Chronic Course in One Limb, Acute Course in the Other. 
The following is a typical example. 

H. R., after having exposed both feet to cold suffered from “cramps” in both legs which 
disappeared in a day or two (1897). A year later there was a recurrence of the pain. These 
indefinite pains persisted for several years, until, in 1902 the typical symptoms of intermit¬ 
tent claudication in the right leg came on, leading him to try various methods of treatment, 
but without avail. Finally, about five years after the onset of the disease, prodromal 
symptoms of gangrene or of trophic disturbances developed in the big toe of the right foot, 
the toe becoming swollen and red, and trophic disorders showed themselves under the nail, 
which was removed, leaving an angry red nail-bed which refused to heal. About the 
same time the second toe also became affected in a similar way. In 1903 the toes were still 
sore, but healed after several months of treatment. Then, after a period of remission of 
three years (1906), trophic disorders developed again in the same place, namely, the big toe 
of the right foot, the pain became very severe, and finally gangrene spread rapidly over all 
the toes necessitating amputation. 

In short, after a period of some nine years, initiated by pain referable 
probably to the deep thrombosis, followed by intermittent claudication and 
trophic disturbances, gangrene finally set in. It is noteworthy, however, 
that several years elapsed between the first attack of trophic disorders and the 
final onset of gangrene. 

History of the Left Leg .—In 1909 intermittent claudication of the leg, then pain and swell¬ 
ing of the toes, bluish discoloration of their tips, the development of superficial ulceration 
of the skin over the anterior part of the dorsum of the foot, gangrene of the fourth and big 
toes, and marked edema of the foot. 

In short, a rather acute case of eight weeks ’ duration. 

11. Relapsing cases may show vessels in which corresponding exacerba¬ 
tions are found in the deep vessels, namely, more recent thromboses and even 
“acute lesions” in the daughter or canalizing vessels. As a rule the free 
intervals are shorter than in the following case. 

A. L. presented a slow clinical course, there being a seven years’ history in a man 45 years 
of age, with sudden onset of cramps in both legs, particularly the right, apparently followed 
by cure of the left leg, there remaining at the time of examination only the absence of pos¬ 
terior tibial pulsation on the left side as evidence of previous trouble. 

After a period of seven years in which intermittent claudication was the chief symptom, 
erythromelia and ischemia in the elevated position were to be elicited, absence of pulsation 
in the posterior tibial and dorsalis pedis arteries, and marked diminution of the angle of 
circulatory sufficiency. Then followed cyanotic discoloration of the big toe and gangrene. 

Similarly, as evidencing the relapsing nature of the malady may be men¬ 
tioned the following. 

S. M. began with pain and coldness in the right big toe with blue discoloration in 1910, 
and trouble with the second toe lasting from April, 1910, to September, 1912, at the age of 


224 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


25, with complete recovery. Now (1913) recurrence of trouble in the big toe of the righ 
foot, swelling and gradual development of gangrene in the lower part of the thigh (total 
duration about three years), leading to amputation August 21, 1913- 


12. Cases with Lethal Outcome— So extensive may the process be, that all the 
extremities are involved. An atrophic condition of the upper extremities may 
ensue from obliteration of the brachial artery. 


I L , male, aged 35, Russian Hebrew, in October, 1906, began with intense pain in the 
left ankle. In September, 1906, an ulcer on the dorsum of the foot was followed iDy progres¬ 
sive gangrene requiring amputation October, 1906. Symptoms then developed in the rig 
leg which became markedly ischemic and extremely painful, so that the. patient begged for 
amputation which was done July 1, 1907, through the middle of the right leg. Neither 
stump healed well, requiring reamputation, there being continued trophic ulcers over the 
stumps of both legs in 1909. On December 17, 1909, there was involvement of the right 
hand, namely marked symptoms of scleroderma or sclerodactyly, atrophic fingers, with the 
brachial artery palpable as a hard cord. 

On April 2^, 1911, the patient was readmitted to the hospital, and the left lower extrem¬ 
ity was again amputated because of failure to heal. On May 25, the patient became lethar¬ 
gic, drowsy, unable to answer questions, and ceased on May 30,i 9 11-1 


In short, this is a case in which both legs were amputated, the right upper 
extremity showing symptoms of scleroderma, marked atrophy, leading to a 
lethal outcome within a period of about five and one-half years. 

13. Cases in the Young with Grave Prognosis.— Just why the disease when 
it affects young men under the age of twenty-five should be apt to take a very 
destructive course is difficult to explain. Many of the cases in the author s 
experience have lost one or both lower limbs within a very short time. 


H K , male, aged 27, Russian Hebrew, had been suffering since the age of seventeen with 
pain in the left foot. In 1905 trophic disturbances appeared so that early in 1906 amputa¬ 
tion became necessary, the leg being amputated five inches below, the knee.. Then m 1906 
symptoms developed in the right leg, pain in the foot and in the big toe which persisted up 

to the present time. , , ,. . , ,, 

Physical examination April 2, 1908, showed a non-healed left stump with necrosis of the 
bone: typical symptoms in the right leg, marked ischemia on elevation, erythromelia, 
absent dorsalis pedis and posterior tibial, and trophic disorder of the big toe. On April 15, 
the big toe was amputated, failed to heal, but amputation was refused. 


So, also, is the following case—one of a youth in whom one would expect 
collateral circulation to become established. 


C. H., American, male, aged 25, had had vague symptoms for some years. Then 
coldness of the left leg. and four or five months thereafter, discoloration of the forepart of 
the left foot were noted. The heel, the big and fifth toes were painful, and trophic disturb¬ 
ances of these toes with gangrene developed after about one and one-half years of definite 
symptoms. The dorsalis pedis, posterior tibial and popliteal arteries of the left leg were 
pulseless, as also the dorsalis pedis of the right leg. .... 

Finally, in January, 1910, amputation took place. This was done eight inches below 
the knee with a poor result, suppuration continuing, due to necrosis of the bone. 

In short, within a period of two years both legs were affected in a boy 
twenty-five years of age, leading to amputation of the left leg, the process 
having been only slightly advanced in the right. 

14. Cases of Long Duration without Trophic Lesions. —Because so many 
years may elapse without manifestations of nutritive derangement of the 
distal parts, the clinical picture devoid of this symptom should be recognized. 
The author’s records show instances where eight to ten, and even fifteen years 
had passed without ulceration or gangrene. The following case may be cited. 

B. H., Russian Hebrew, male, aged 47, seen October 19, 1910, began eight years ago 
with pain on walking, intermittent claudication, one year later manifestations of migrating 

1 This case because of its importance is discussed more fully on p. 372. 


THROMBO-ANGIITIS OBLITERANS—CHRONIC STAGE 


225 


phlebitis, and for about one year the feet have been cold. Six years ago he noticed dis¬ 
coloration of the feet. 

On physical examination both feet were found to be involved with the typical symptoms, 
erythromelia and ischemia, the left being more marked both as regards erythromelia and 
ischemia, than the right. On the right, the dorsalis pedis and posterior tibial were pulse¬ 
less; on the left, pulsation was absent in these vessels as well as in the popliteal. 

Here is a case of long standing in which the trouble dated back farther 
than the history would indicate, with involvement of both legs after an eight 
years’ course, with development of all the typical symptoms up to the stage 
in which ulceration was imminent. 

15. Cases with All Extremities Involved. —Not unusual is it to note that 
both upper extremities may participate in the process, although the de¬ 
structive force of the vascular occlusion makes itself but slightly felt in the 
upper limbs (Chap. LIX). 

M. F., Russian Hebrew, aged 34, began at the age of thirty with pain in the right 
foot. This was followed by numbness of the right hand. Six months ago symptoms 
were observed in the left foot, such as coldness and pain on walking. 

On physical examination it was found that the right hand and left leg were distinctly 
involved, there being atrophy of the right hand and coldness of the fingers with a faint 
radial pulse. The left foot showed evidences of involvement, rubor, coldness and absent 
dorsalis pedis and posterior tibial. 

Five years after the onset of symptoms in the left leg, the second toe became gangren¬ 
ous. The foot was in a state of marked erythromelia, and the pulsations in the posterior 
and anterior tibial arteries were absent. Gritti-Stokes amputation was done with good 
result. 

Eighteen months after the amputation of the left leg, the patient complained of intense 
pain in the calf of the right leg accompanied by the formation of an ulcer on the foot. The 
symptoms progressed and conservative amputation was done below the knee. However, 
owing to the persistence of an ulcer on the right stump for 6 months, Gritti-Stokes amputa¬ 
tion was finally resorted to with complete abatement of all the symptoms. 

Two years after the last amputation the patient gave evidences of involvement of the 
left upper extremity, in the presence of pain and coldness of that part. The left radial pulse 
was found imperceptible, the right barely palpable. 

When last seen (September 8, 1922) the patient, who has been addicted to morphine 
was free of all symptoms, the left radial pulse, however, being imperceptible. 

16. Cases with Pain Only. —-Recognition depending on objective signs are 
amongst those usually undiagnosticated. There are no trophic disorders. 
The patients usually have been treated by an orthopedist, but the ischemia, 
rubor and pulseless vessels should direct attention to the true nature of the 
malady. 

M. N., Russian Hebrew, aged 35, presented a picture of thrombo-angiitis obliterans 
without trophic disturbances, simply marked ischemia, moderate erythromelia after a 
period of indefinite pain which had been diagnosticated as due to flat foot. The arteries of 
both legs failed to pulsate. 

17. Cases without Trophic Disorder or Gangrene Requiring Amputation .— 
There have been a number of cases in our experience, either with one or both 
limbs affected, that suffered such agonizing pain for an extended period of 
time, that they vehemently begged for amputation, which was carried out in 
several instances. The following may be cited as an example. 

H. R., August 6, 1916, born in the United States, Hebrew, began to experience pain 16 
months previously in the calf of the left leg, the pain extending downward over the entire 
leg and foot, especially over the toes. The pain was severe, cramp-like in character, 
intensified by walking, diagnosticated as due to flat feet. There was a history of migrating 
phlebitis of both lower extremities a year previously. 

Physical examination, August 6, 1916. The left foot was markedly cold and somewhat 
smaller (atrophic) than the right, and in a state of chronic rubor, most marked in the 
pendent position. On elevation there was intense pallor, on depression marked congestion 
15 


226 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


erythromelia, and rubor. None of the pulses, neither the dorsalis pedis nor posterior tibial 
arteries were palpable. 

Diagnosis.— Thrombo-angiitis obliterans without trophic disorder or gangrene. 

The patient was kept under observation for some 12 days, and his supplication to have 
the limb removed was finally acceded to. 

At operation, August 18, 1916, amputation of the left leg (Gritti-Stokes), most of the 
arteries were found closed, the popliteal also being filled with organized thrombus. The 
popliteal veins were open. 

18. Cases with All the Vessels Pulsating. —These will be described in * 
more detail under Borderline Cases (Chap. CIV). Clinical and pathological 
investigations have demonstrated that an atypical clinical picture with 
predominating vasomotor symptoms, or even the typical picture of thrombo¬ 
angiitis obliterans may be produced, when the vascular lesions are confined 
to the territory of the plantar or the digital vessels, with occasional involve¬ 
ments of the distal parts of the dorsalis hallucis. The symptoms may begin 
with vague pains in the feet to which little attention is paid, or coldness of 
the toes. Later on this pain becomes severe, is referred to one or more toes, 
and is followed by cyanosis or rubor, or a combination of both. Or, the pain 
may be slight, and the coldness and cyanotic discoloration may be noteworthy. 
In the latter case the clinical picture may simulate that of some of the vaso¬ 
motor neuroses. When pain is marked, a diagnosis of incipient or 
restricted vascular occlusion can be made with a fair degree of certainty. 

M. C., Russian Hebrew, consulted me on the 7th of July, 1911. He was devoid of 
symptoms until 2 weeks previously, when he suddenly began to experience pain in the 
whole left foot. At first the pain was slight, but became gradually more and more severe. 
After a week the toes became red without being preceded by any ischemia. Since then the 
third toe has become blackish and ulcerated, and now the pain is intense by day and night. 

Physical Examination.—Left foot shows discoloration of the third, fourth and fifth 
toes, these being cyanotic. The fourth toe is reddened. On the inner side of the tip of 
the middle toe there is a patch of superficial gangrene of the skin about the size of a ten cent 
piece, the center being ulcerated. The tip of the toe is very cyanotic, suggestive of impend¬ 
ing gangrene. On elevation of the foot the visible veins become empty, the third, fourth 
and fifth toes slightly bluish, but no distinct blanching can be elicited. 

All of the vessels of both extremities pulsate normally. 

Conclusion: Although an absolute positive diagnosis could not be made in 
this case, since amputation was not done, a number of other similar cases 
have shown conclusively that the clinical picture represented occlusive 
thrombo-angiitis obliterans confined to the territory of the plantar and digital 
arteries. 

19. Cases with Marked Involvement of the Upper Extremities are discussed in 
full elsewhere (Chap. LIX). 

20. Cases with Migrating Phlebitis are of such importance as to warrant 
special consideration later on (Chap. LVIII). 

21. Cases in Females. —So rare is the disease in females, that doubt has been 
cast on the possibility of its occurrence outside of the male sex. The author 
has observed but 3 cases that were clinically indistinguishable from typical 
thrombo-angiitis obliterans, but since amputation did not become necessary 
in any of them, pathological confirmation is missing. 

Raynaud’s syndrome in elderly women with arteriosclerotic vessels or 
acrocyanosis may give confusing clinical combinations, that should be care¬ 
fully differentiated from thrombo-angiitis obliterans. 

A case that belongs clinically to thrombo-angiitis is the following. 

M. D., female, American, seen February 2, 1912, parents Bavarian Jews, was always 
perfectly well except for “sciatica” in October, 1911, possibly related to her present trouble. 
About this time she had an attack of pain in the right thigh and foot which was so severe 


THROMB 0 -ANGIITIS OBLITERANS—CHRONIC STAGE 


227 


that she was kept in bed for two weeks. The diagnosis was “sciatica” from which she 
apparently recovered, but discomfort and even pain remained in the right sole and instep. 
The right foot, too, seemed much colder than the left, not bluish but pale at times, always 
appearing whiter than the left foot. After walking about one block, the pain would become 
so intense that she had to stop and rest. 

In short, an indefinite history of sciatica followed by pain in the foot, coldness, pallor and 
intermittent claudication. 

Physical examination, February 2, 1912, revealed the absence of the dorsalis pedis 
pulse of the right foot, a doubtful posterior tibial, all the other vessels of both sides pulsat¬ 
ing. On elevation the right foot showed moderate ischemia. Examination of the sensory 
nerve condition was negative. 

Diagnosis: A case of thrombo-angiitis obliterans with moderate erythromelia of the 
right foot in the dependent position, ischemia on elevation, absent dorsalis pedis with a 
history of pain in the foot, ankle and sole following sciatica. 

The patient was not seen again until some four months later, when in June, 1912, the 
following history was taken. Since the last examination she had been receiving hot air 
treatment, which she believed caused a burn. An ulcer developed under the big toenail of 
the right foot, the nail subsequently falling off. The nail-bed healed after four weeks. 
About February 16, the foot became very bad, the toes looked almost black, so that in 
March after several consultations with surgeons amputation was advised. The big toe 
particularly seemed affected being bluish black, the bed of the nail having become gangren¬ 
ous. Certain ointments were used, the symptoms gradually subsided, amputation was 
refused, and healing took place. 

June 19, 1912, physical examination of the right leg in the horizontal position showed 
cyanosis of the big toe, with a deformed nail. There was slight erythromelia of the fore¬ 
part of the foot in the dependent position, marked ischemia on elevation, especially over 
the sole, less over the dorsum of the foot. A fairly marked reactionary erythromelia was 
produced when the foot was returned to the horizontal, and absence of pulsation of the 
dorsalis pedis and posterior tibial arteries was noted. 

In short, since the last examination the patient developed trophic disorders which were 
probably not at all related to the hot air treatment, and might have come on spontaneously; 
erythromelia had become more marked, as also ischemia, and the dorsalis pedis and pos¬ 
terior tibial were definitely occluded. 

The patient was again seen on January 4, 1913, when both feet were slightly cold with¬ 
out evidences of atrophy. In the pendent position the right foot showed definite rubor. 
On elevation both feet showed distinct blanching and there was distinct reactionary erythro¬ 
melia of the right leg after elevation. The dorsalis pedis and posterior tibial arteries of the 
right were not palpable, as well as the dorsalis pedis of the left foot. 

Summary: January, 1913, although the process had not progressed much in the right 
leg, the left leg also seemed now to be involved. 

June 10, 1913, the patient said the right foot had become distinctly warmer, and she 
considered herself much improved being able to get about much better. Physical examina¬ 
tion showed the same condition of the pulses as at the last examination. The right foot 
showed marked erythromelia, the left but slight, both evidencing distinct ischemia on 
elevation. 

The following case may be cited as another example of thrombo-angiitis 
obliterans in a female. 

A. C., 38 years of age, began with pain in the calf of the right leg upon walking following 
an attack of influenza 2 years ago. The right leg became swollen, but after 6 months the 
cramps in the calf disappeared, the swelling, however, persisting accompanied by numbness 
of all the toes. Eight months ago the right foot became cold, and the patient noticed a red 
spot on the inner aspect of the right leg. 

Physical examination reveals edema of the right foot and leg, more marked over the 
ankle. The great toe is hemorrhagic, showing evidences of discoloration of the tip with 
ecchymosis. There is moderate erythromelia over the forepart of the right foot. Elevation 
elicits considerable ischemia. Upon return to the horizontal position, the color does not 
return for some time, rubor appearing first above the roots of the toes, the toes themselves 
remaining ischemic and cyanotic. 

The dorsalis pedis and posterior tibial pulses of the right foot are absent, those of the 
left present. 

In short, thrombo-angiitis obliterans in a female, with involvement of the 
right lower extremity, the chief symptoms being erythromelia, ischemia and 
absent pulsations. 


228 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


22. Cases in Elderly Individuals will offer difficulty in differentiation from 
sclerotic vascular diseases all the more so since the two conditions may co-exist 
simultaneously, the latter usually engrafted upon the former when in 
the silent, latent, or anatomically “healed” stage. Autopsy findings (Chap. 
LXIII) have convinced the author that the arteries are particularly prone to 
lesions of atherosclerosis, although the territories involved with thrombo¬ 
angiitis obliterans may be least or not at all affected. 

There is a series of cases in which the symptoms apparently become severe 
after the age of forty. In these, a careful search into the history will reveal 
the fact that there had been symptoms many years previously, and in all 
probability the disease had come to a standstill. Therefore, in view of this 
fact we must give a rather guarded prognosis in all cases of thrombo-angiitis 
obliterans that apparently heal. Our experience with cases in young men 
between twenty-five and forty years in whom complete cessation of all 
manifestations takes place, confirms the diagnostic assumption of the previous 
existence of the disease in some of the older arteriosclerotic individuals. 

Pathological pictures afford the anatomic corroboration for the coincidental 
occurrence of the two affections. 

23. Cases with Apparent Healing or “Cure ”—Clinical inactivity, abate¬ 
ment of pain and intermittent claudication, improvement in ability to walk 
and the absence of trophic lesions are interpreted by the patient as indicating 
subsidence of the disease, usually in the words “my legs give me no more 
trouble.” That such a free interval is to be regarded under all circumstances 
as of doubtful duration, experience has taught. An interruption by a repeti¬ 
tion of the manifestations in the other limb is not uncommon as elsewhere 
described. 

In the period of clinical inactivity, however, the existence of the disease 
should not escape our observation, since slight ischemia, or some rubor or 
reactionary rubor, or a diminished angle of circulatory sufficiency and pulse¬ 
less vessels can be demonstrated, these signs in varying combinations and 
degree of intensity. 

One of the most exquisite examples of apparently complete clinical cure 
of a case in which trophic disorders had been present, and imminent gangrene 
of one limb had impelled a surgeon to advise amputation, is afforded by the 
following case. 

J- R> Russian Hebrew, aged 32, consulted the author September 9, 1909 to ascertain his 
condition, since his brother had the same disease and was developing gangrene. In 1894 
(at the age of seventeen) he began to experience a peculiar cutting pain in the left calf on 
walking a short distance, so that he had to drag the limb. This symptom (probably 
intermittent claudication) persisted for about two years during which time he often could 
not sleep at night because of the pain and burning in the toes. In 1896 the case was 
diagnosticated as erythromelalgia, for at that time his leg was very red. The right leg , on the 
other hand, at no time gave him any symptoms. Another surgeon about this time made the 
diagnosis of flat foot and put the foot in a cast for two weeks. After the cast was taken off, 
a sore developed on the inner side of the left ankle which refused to heal (decubitus?). In 
spite of all the measures taken to bring about the healing of this ulcer, the wound was still 
open one year after the removal of the cast. At that time, the symptoms were so intense 
that he was advised to have the limb amputated, but refused, and a year later the wound 
spontaneously closed with the use of ichthyol dressing, and gradually after this time (1898), 
four years after the onset, all the symptoms left him, and he has been free from trouble ever 
since. 

September n, 1909, one year after the wound closed, he was examined by the author, 
and all the vessels of both lower extremities, including the femorals, popliteals, posterior tibials 
and dorsalis pedes were found pulseless. Both feet showed a very slight rubor in the pendent 
position, but not of sufficient amount to be diagnosticated as erythromelia. Besides this, 
there was distinct ischemia in the elevated position, but not at all marked. There were no 


THROMBO-ANGIITIS OBLITERANS—CHRONIC STAGE 


229 


trophic disturbances , the patient complained of no pain, and considered himself perfectly 
well. There was no intermittent claudication, nor any symptoms referable to the lower 
extremities. 

In short, we have here a case of typical thrombo-angiitis obliterans in the 
left limb, spontaneously “cured” as far as symptoms are concerned, in spite 
of the fact that extensive obliteration of vessels had occurred. There seems 
to be no question but that the disease must have been present in the right 
limb also, although at no time did the patient discover any symptoms. 

The following history is suggestive of the presence of lesions in one limb, 
that however, spontaneously healed. 

A. L. gave a history of cramps in the left leg as well as in the right, and on examination 
seven years later marked symptoms of thrombo-angiitis were found in the right leg. In the 
left, the only symptoms of the disease were the absence of pulsation of the posterior tibial 
and at times cyanosis of the big toe in the dependent position. Therefore, all the symptoms 
had subsided, these two signs being the only ones left indicative of previous trouble. 

Some cases may go along for a year with the development of gangrene 
of one toe and trophic disturbances, as well as all the usual symptoms, and 
then spontaneously after hot air or postural treatment show complete 
subsidence of all symptoms. Such a case was the following. 

H. G. developed gangrene of the big toe after a year of the usual pains and intermittent 
claudication (December, 1910). This gradually healed while he was treated in January, 
I 9 II > by the hot air method, and remained perfectly well under our observation for four 
years, so that when the patient was seen in December, 1914, the left foot, although present¬ 
ing a somewhat atrophic appearance, an absent dorsalis pedis and posterior tibial pulse, was 
found otherwise in fairly good condition as far as circulation was concerned, and presented 
no symptoms whatever. 

Some of our cases were observed for several years, and although at times 
there was slight exacerbation, many of them showed no tendency to marked 
progression or to the development of gangrene, so that they could be regarded 
as stationary or clinically “cured.” As, 

A. G., was observed from November 27, 1908 to May 9, 1911. He had had a typical 
history of intermittent claudication of the left leg, followed after two years by pain 
in the region of a trophic lesion. This spontaneously healed, and when the patient was seen 
in 1908 there were definite evidences of involvement of both legs with a history of pain on 
walking, coldness of the foot, thin condition of the foot, and numbness with occasional 
whitening or pallor of the foot on walking. Although the patient was seen and carefully 
examined some four or five times a year, no aggravation of his condition was noted, no ulcers 
developed, and the case was regarded in 1911 as being a stationary one, the cyanosis, the 
pulseless vessels, the tendency to coldness and numbness of the feet persisting. 

In short, we have here a proof of the fact that six years may elapse with¬ 
out any marked destruction of parts, and without gangrene. 

24. Arrested Stage or Temporary Healing in Thrombo-angiitis Obliterans. 
Surprising changes both for the worse and for the better are the impressive 
features of the variegated clinical picture of thrombo-angiitis obliterans. 
So, we occasionally are confronted with a stage of threatening gangrene 
of the leg which limits itself and becomes restricted to the disintegration 
of but a part of a phalanx or less. Or, one may observe the complex— 
ischemia, rubor, pain and trophic disorders—all disappear with its subjective 
symptoms, the patient believing himself cured as far as the previously 
affected limb is concerned. When we encounter such cases during a period 
of renewed morbid activities in the other extremity, the residual diagnostic 
features such as atrophy and pulseless vessels can be appreciated and given 
deserved consideration. Periods of remission, arrest of symptoms with 
either none or very slight manifestations may last for years, but the possibility 


230 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


and probability of an exacerbation leading to eventual loss of the limb must 
be borne in mind, since such an issue is extremely common. 

A good illustration of such subsidence and practically complete abate¬ 
ment of circulatory disturbances is worthy of attentive contemplation to 
aid in both diagnostic and prognostic conception of the malady. So we will 
cite the case of 

Typical thrombo-angiitis obliterans of the left leg , gangrene of toe, “healing” or arrest and 
disappearance of symptoms, followed by involvement of the right leg, four years after cessation, 
relapse and extension of lesion in the left leg. 

H. G., male, Hebrew (born in Turkey) age 39 years, examined December 10, 1910, 
smoked fifteen Turkish cigarettes a day beginning at the age of fifteen. The diagnosis of 
flat feet was made ten months ago when he had pain in the left calf, also the diagnosis of 
“rheumatism.” He then used plates for the left foot. There was pain in the left calf on 
walking three to four blocks. No history of migrating phlebitis could be elicited, and the 
right leg was free of symptoms. 

Five weeks ago there was pain in the left big toe, and four weeks ago redness. For the 
past week a black spot had been seen on the outer side of the left big toe. Now the 
patient has most pain in the big and second toes, particularly at night, sleeping only a 
couple of hours. 

Physical Examination.—December 10, 1910, the left foot is in a state of chronic ery- 
thromelia, and the big toe shows a dry gangrenous patch on the outer side 1 cm. in diameter, 
the rest of it being cyanotic. 

The iliac, femoral and popliteal arteries of both legs were found pulsating, the posterior 
tibial and dorsalis pedis pulses of the right leg palpable, those of the left not. 

There was a moderate increase of the erythromelia in the pendent, moderate ischemia in 
the elevated position. 

On January 1, 1911, there was still an ulcer about one-half inch in diameter on the big 

toe. 

On March 14, 1914 the following history was obtained. Since early in 1911 the left leg 
had given him no more concern, and since the healing of the ulcer, all symptoms vanished. 
For two months, however, the right leg had been troubling him with a sensation of pins in 
the sole of the foot, so that he had to rest at every block, and when he walked the pain 
ascended into the right calf. The right foot, too, had been discolored in the forepart. 

Physical Examination (March, 1914).—The right foot is bluish red, the toes being most 
involved. The dorsalis pedis and posterior tibial do not pulsate, the femoral does. The 
left foot, which is now without symptoms, has a somewhat atrophic appearance, but is 
negative except for the absent dorsalis pedis and posterior tibial pulses. 

On elevation it is very evident that the circulation of the right foot is worse than that of the 
left. This can be seen particularly over the sole, where the right foot takes on a greenish 
white appearance with the small toe cyanotic. If we press the other toes, those of the 
right foot show very little blood, and that which is present is of a purplish tint, whereas 
on pressing the toes of the left foot, considerable red color is in evidence. During the 
period of elevation even the dorsum of the right foot became markedly blanched. 

On putting the foot back in the horizontal position, the return of color is seen as a 
mottling over the right foot, the toes being the last to regain their color. 

In the pendent position the return of blood in the right foot makes it intensely red, the 
rubor extending somewhat above the ankle. 

In short, four years after our first observation, the left foot was found (March 14, 1914) 
in an arrested or temporarily healed state, the right previously normal, then actively 
implicated in the disease. 

October 27, 1914, the right foot has the intense red look and the puffy appearance of the 
old chronic cases. In the pendent position, the erythromelia deepens rapidly and then 
cyanosis comes on. The fourth toe, the distal phalanx of which is already separated, shows 
a gangrenous area of skin. The fifth toe is completely absent and the foot is very cold. 
The pain seems to be relieved in the pendent position. 

When again seen on January 15, 1915, these notes were taken. The patient feels better 
now, but still has intermittent claudication in the left leg, and pain between the third and 
fourth toes of the right foot, where there is a patch of gangrene. 

Both feet are in a state of chronic erythromelia, the right more marked than the left. 
The right foot is somewhat enlarged, the toes slightly swollen, so also the dorsum. Where 
the fifth toe spontaneously separated, the wound has healed. The site of the separation of 
the terminal phalanges of the fourth toe of the right foot still shows a dry smooth patch. 
In the horizontal position there is practically no erythromelia of the left foot, and only slight 
of the right, but in the pendent position both feet show fairly marked erythromelia. It is 


THROMBO-ANGIITIS OBLITERANS—CLINICAL PICTURE 


231 


noteworthy that the left foot shows this erythromelia although there are no trophic dis¬ 
turbances/ The dorsalis pedis and posterior tibial of both feet are pulseless. He has no 
pain when at rest. On elevation there is marked blanching of the left foot, slight of the 
right. 

In brief, four years after establishment of the quiescent stage in the left foot, afresh exacerba¬ 
tion with recurrence of erythromelia, ischemia and pain. 

25. Doubtful Cases . 1 —Such a group is but a clinical and arbitrary segrega¬ 
tion of cases, the exact nature of which may seem questionable, at least 
during a part of their clinical course. Because of the absence of pathog¬ 
nomonic symptoms during the early stages of certain cases of thrombo¬ 
angiitis obliterans, and because of the association of vasomotor symptoms 
in others, enough data for any other than a presumptive diagnosis may fail 
to be at hand. 

To divorce the following clinical complex altogether from thrombo-angiitis 
obliterans and to make a symptomatic diagnosis of intermittent claudication 
as has been done by Erb and others, would be tantamount to a relinquishment 
of every desire to aim at a pathologic differentiation. Confronted with a 
case of cramps or pain in the legs or feet on walking, without static cause, 
without any history of migrating phlebitis, without either ischemia, rubor 
or pulseless vessels, we may be allowed to suspect that thrombo-angiitis 
obliterans is developing, and that it has as yet affected none other than those 
arteries that are beyond the reach of palpation— e.g. the distal branches of 
the anterior tibial and the plantars. To extend the designation of inter¬ 
mittent claudication so as to denote a possible clinical and pathological 
entity, would be subversive of all modern attempts to clarify clinical con¬ 
cepts. For, intermittent claudication, as has been elsewhere lucidated, 
should be restricted so as to indicate coordinate manifestations; that is, a 
“symptomatic association,” and not a “symptom complex,” when the latter 
appellation is used as the equivalent of a morbid unity. So we may allow 
such patients to constitute a group entitled “Thrombo-angiitis obliterans 
with latent (larvata) or undeveloped physical signs.” 

This variety must not be confounded with that already alluded to, in 
which a patient is unaware of the disease, that is, “ Thrombo-angiitis obliter¬ 
ans without subjective symptoms.” For, in the latter no complaint is made, 
whilst amongst the instances belonging here, the patient’s discomfort may be 
great. It is merely an insufficiency of pathognomonic objective signs that 
warrants this classification. 

Amongst the various cases encountered are the following: 

(a) Intermittent claudication only with absolutely no objective signs; 

(b) Coldness and cyanosis of the toes, possibly with local pain; but the 
physical signs of thrombo-angiitis obliterans absent. 


CHAPTER XLIII 

THROMBO-ANGIITIS OBLITERANS—CLINICAL PICTURE 

Classification. —For purposes of clinical diagnosis it is useful to divide the 
cases of thrombo-angiitis obliterans into four groups. 

I. Typical thrombo-angiitis obliterans of the lower extremities. 

1 Vide also Chap. CIV. 


232 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


II. Thrombo-angiitis obliterans with associated thrombo-phlebitis or 
migrating phlebitis. 

III. Thrombo-angiitis obliterans with involvement of the upper extremi¬ 
ties. 

IV. Thrombo-angiitis obliterans with secondary or complicating athero- 
or arteriosclerosis. 

It must be remembered, however, that this grouping is artificial, for 
many cases may belong to one or more of these subdivisions at the same time. 
Thus, cases in group I may be affected with migrating phlebitis, or may have 
symptoms of thrombo-angiitis obliterans of the upper extremities. The 
classification is helpful for description and study. 

For purposes of treatment it is often useful to divide the cases according 
to the stage of the development of symptoms at the time of clinical observa¬ 
tion, into 

1. The prodromal stage, that of intermittent claudication (sometimes 
with migrating phlebitis). 

2. The stage of trophic disorders and gangrene. 

1. TYPICAL THROMBO-ANGIITIS OBLITERANS OF THE LOWER 
EXTREMITIES. —The clinical picture varies considerably, depending upon 
the duration of the disease when the patient is examined, the severity, the 
effects of exposure, traumatism and complications. The following case 
types may facilitate the recognition of the disease, although they must not 
be considered as exhaustive. They should be recognized, since they are 
in most instances but the prodromal manifestations of gangrene. 

A brief exposition of some of the typical forms of onset (A) of the malady 
in the lower extremities, and short summaries of some of the more usual 
clinical pictures (B) as they are developed under our observation, may serve 
to clarify our concepts of the effects of the morbid lesions in the vessels. 
/ A. Forms of Onset, i. Onset with Intermittent Claudication. —This 
symptom-complex need not be discussed in detail since it has been described 
elsewhere. 1 But allusion may be made to its importance as one of the first 
manifestations of the disease. Very frequently it antedates by weeks, 
months or years, the other symptoms—the rubor, the coldness, the cyanosis, 
the blanching, the migrating phlebitis and trophic lesions. It may succeed 
the attacks of phlebitis or the attacks of pain referable to the deep vessels. 
And, it may be regarded as of such negligible character by the patient, as to 
escape his notice, whenever more serious phenomena such as ulcers and 
exquisite local pain in a toe render it comparatively insignificant. On the 
whole, it is a sign of such distinctive character, as to be regarded as am 
important and integral part of the clinical picture. 

2. Onset with Symptoms Referable to the Deep Vessels (Acute Stage). —In a 
number of cases there is a history of a rather sudden onset, with attacks of 
severe pain in the calf of one of the legs, without demonstrable cause, and 
attributed by the patient either to exposure to cold, or to severe exercises, 
or, described as coming on without reason. In a number of such cases symp¬ 
toms of intermittent claudication developed somewhat later, but the history 
of acute symptoms was so definite, that is seemed reasonable to conclude 
that they bore some relation to the occurrence of thrombosis in the deep 
vessels (Chap. XLI, p. 219). 

Quite a number of cases describe the onset as being sudden, with pain in 
the calf and foot made worse by walking. After a time, the acute symptoms 


1 Chap. XXVI. 


THROMBO-ANGIITIS OBLITERANS—CLINICAL PICTURE 233 

give way to a recurring cramp or pain of moderate severity brought on bv 
walking (intermittent claudication). It is more than likely that in many of 
these cases this acute onset marks the inflammatory stage of the disease in 
the deep vessels and is followed by the stage of intermittent claudication, 
where the pain is dependent upon circulatory deficiency. 

It is quite a difficult matter in all cases to get a definite history of the onset 
of the disease. If the hypothesis regarding the relationship between the 
symptoms and the occurrence of the thrombosis of the deep vessels is correct, 
namely, that certain attacks of cramp-like pain in the calves and in the legs 
may accompany the real onset of the disease, we should be able to elicit such 
a history in most of the cases. However, this is not possible. If we take 
into consideration the type of cases with which we are dealing and the lack 
of intelligence of some of the patients, their failure to properly estimate and 
recall symptoms occurring many years back, will not be surprising. 

Then, as for the symptoms which do not really belong and are really not 
due to the onset of the pathological lesion, we may say that these also vary in 
their incipiency. In some of the cases there is no question but that the disease 
seems to begin with symptoms of intermittent claudication. In some others, 
however, we were unable to obtain such a history, for the patients referred 
their pain to the foot or to the toes, and particularly to those toes or that 
toe which very soon becomes the seat of trophic disorder or gangrene. In a 
certain case there was a history of pain in the fifth toe of the right leg at the 
very beginning of the disease. Two weeks later ulceration took place and at 
the end of the month the toe was amputated for gangrene. 

If we carefully analyze such a history, we cannot doubt but that the pain 
complained of was that of the impending trophic disorders and gangrene. 
It is more than likely that other manifestations had initiated the real begin¬ 
ning of the disease, but had remained unnoticed. 

3. Onset Overlooked, Trophic Lesions First Noted. —In the careless, ignorant 
hyposensitive individual, the first indication of trouble may be the development 
of an ulcer or even a patch of gangrene; or, exquisite pain in a toe, usually 
the forerunner of serious nutritional disturbance is the first noticeable 
manifestation. 

Careful scrutiny of many of the histories demonstrates conclusively that 
the onset of the disease is often overlooked. In some cases, we find that one 
toe has been amputated, and in eliciting the history, we find that a sore had 
developed many years ago without cause, leading to spontaneous gangrene 
and finally amputation. Thus, in one case the history states distinctly 
that fifteen years previously the big toe of the left foot was amputated for 
spontaneous gangrene, the patient remembering no other symptom asso¬ 
ciated with it other than the local pain. 

4. Onset Overlooked until Second Leg Affected. —In the chapter on the 
Course of the Disease, the latency of the affection and the insidious manner in 
which it may implicate one extremity, wholly unknown to the patient, have 
been discussed. Here, it may be permissible to emphasize merely that a 
medical examination should not disregard the following signs of arterial 
involvement in a limb, that apparently gives the patient no concern; namely, 
absent dorsalis pedis or posterior tibial pulses, with or without rubor or 
ischemia, and coldness of a portion of the periphery or cyanosis. When 
merely one pulseless vessel is the only apparent objective sign, careful 
search for reactionary rubor and for ischemia after repeated and prolonged 
elevation may be rewarded by positive findings sufficient to warrant the 
diagnosis. 


234 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


5. Onset with Coldness and Cyanosis .—The symptoms to which the prac¬ 
titioner is wont to give too little heed are coldness and blueness of one or more 
toes with or without pain. It is true, other manifestations wholly ignored by 
the patient may precede, but it is for the signs of discomfort that the patient 
seeks relief. If a routine examination according to the principles laid down 
be followed, an early diagnosis may be made. 

6. Onset with u Rheumatic Pains ”—Pain described as such, when 
referred to the ankle, the foot or the tibia, and when not typical of intermittent 
claudication, is a symptom whose significance may be underestimated. 
This dictum may be safely accepted, that in a young Hebrew , especially of 
Russian or Polish origin , any persistent discomfort in the foot or leg justifies 
careful investigation as to the integrity of the arteries of the limb, because of the 
manifold variations in the symptomatology. 

B. Usual Clinical Pictures. —Some of the more common clinical manifes¬ 
tations group themselves in our experience as follows: 

1. Symptoms of intermittent claudication, namely, pain in the calf of 
the leg or in the foot, made worse by exercise and walking, may last for a 
variable period of time, and then distinct rubor or erythromelia develops, 
the picture being a combination of these two chief symptoms. 

2. Symptoms of intermittent claudication may predominate for long 
periods, may remain unrecognized, but should be regarded with suspicion if 
they are accompanied by blanching of the foot upon elevation, rubor upon 
depresssion of the foot after elevation, and loss of pulsation in the dorsalis 
pedis, possibly posterior tibial, or both, or even the popliteal arteries. 

3. Symptoms of pain or intermittent claudicationj may give way after a 
variable time to trophic disturbances, ulcers, fissures, hemorrhagic blebs, 
scaling of the skin, etc., but when these are present, the typical phenomena 
elicited by physicial examination are regularly to be found. 

4. Thrombo-angiitis obliterans may develop silently in one limb without 
symptoms, indefinite signs of pain, indefinite intermittent claudication having 
been present and having been unnoticed or undiagnosticated, being only 
elicited when the patient seeks advice for characteristic symptoms of 
thrombo-angiitis obliterans in the other limb. Physical examination will 
reveal absence of pulses, in one or both limbs. 

5. The symptoms of thrombo-angiitis obliterans may develop in 
an orderly and typical sequence, namely: first, stage of indefinite pains or 
intermittent claudication; second, stage of rubor or erythromelia, with absent 
pulsations, and ischemia on elevation; third, a stage of trophic disorder; 
finally, a stage of gangrene. 

6. Cases may pass through any of these stages and the progress of the 
disease may become arrested spontaneously, or with treatment. Those in 
which the signs of intermittent claudication and pain alone have developed, 
will regularly show upon examination the ischemia on elevation, or at least, 
some reactionary erythromelia, absent pulse in at least one of the larger peri¬ 
pheral vessels, such as the dorsalis pedis and posterior tibial, or often both. 
When the disease comes to a standstill, the subjective symptoms disappear, 
but the objective may persist for a long time, that is, the ischemia on eleva¬ 
tion, the absent pulses and the erythromelia. In some of these, however, 
even the ischemia and the reactionary erythromelia may become absent, the 
pulseless vessels alone remaining as indications of the disease. When ery¬ 
thromelia becomes marked, it is likely to persist for a long time, even after 
the disease is spontaneously arrested, or apparently cured by treatment. 


TH ROM BO-ANGIITIS OBLITERANS—APPEARANCE OF THE LIMB 235 


When trophic disorders develop, the pain is wont to become severe. 
Ulcers may spontaneously heal; the pain may leave the patient; the inter¬ 
mittent claudication may abate, the ischemia and erythromelia being the 
last phenomena to disappear. 

Those patients with gangrene who become spontaneously cured, pass 
through the stages indicated above, the typical phases of mortification, 
involving as a rule only small portions of a toe, or a toe, being followed by a 
long period of convalescence, lasting months or even years, and resulting 
finally in cure. In these, too, the pulseless vessels will tell the tale, erythro¬ 
melia persisting for a long time. 

7. The Chronic or Incurable Ca§es.—These are common, the disease in 
most instances being a progressive one. The advent of the various stages, 
although often delayed may be expected to develop. In the chronically 
progressive type, amputation may become necessary, either in the stages of 
trophic disorder, or gangrene. The pain may be so excruciating that sleep 
is impossible, amputation finally being the last resort, even though the 
lesions are merely those of ulceration with or without infection; or, the 
control of pain in cases of gangrene may also be impossible, amputation being 
the only method of obtaining relief. 

8. Cases in which any of the above symptoms or complexes may affect 
first one lower extremity, then the other, possibly abating in the extremity 
first involved, and making more marked progress in the other. There 
are cases in which one or both lower extremities are involved, and in the 
further course of the disease one or both upper extremities also give mani¬ 
festations of the same affection. These will be considered under the group— 
Thrombo-angiitis Obliterans of the Upper Extremities. 

9. Fulminating Cases—Although the regular course of the disease is a 
chronic, progressive one with a long prodromal period, there are cases 
in which (according to the histories) very rapid development of gangrene can 
take place. It is possible that the prodromal phenomena were unnoticed, 
being of slight degree, or developing insidiously. In these patients coldness 
of the foot and pain in the toes may be the first symptoms, leading rapidly to 
areas of mortification. 


CHAPTER XLIV 

THROMBO-ANGIITIS OBLITERANS—APPEARANCE OF THE 

LIMB 

Since the special and more or less striking deviations in the appearance of 
limbs affected with thrombo-angiitis obliterans are to be described sepa¬ 
rately, there remains to be mentioned here only those general peculiari¬ 
ties of color and conformation that cannot be classed into single categories, 
but that are the result of a combination of factors, partly nutritional, partly 
compensatory tissue growth, partly adaptation, and partly circulatory 
derangement. 

Leaving out of consideration, then, the appearance of the extremity when 
it is discolored into marked pallor (ischemia), rubor (erythromelia, hypere¬ 
mia), or cyanosis (asphyxia, lividity), when changed because it harbors 
trophic ulcers and infections or gangrene, then there are still at hand 


236 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


certain peculiarities that are the more or less characteristic products of the 
many factors at play in this disease. 

For our diagnostic purposes, it is true, our inspection should be concen¬ 
trated first and foremost on the more striking,alterations above reviewed; 
but for special differentiation, even minor changes are of no mean import. 

In the cases with but few symptoms, with pain or intermittent claudica¬ 
tion predominating, there may be nothing worthy of note other than dys¬ 
trophic alterations in the nails; or even these may be absent. When, how¬ 
ever, rubor has existed for some time, and more particularly when trophic 
lesions have been or are present, the gross appearance of the foot undergoes 
distinct changes. These vary in intensity and extent. It is very common to 
not a peculiar thickening of the subcutaneous tissues that differs from edema 
and that corresponds to chronic lesions under the skin. Through this the 
normal markings as expressed by the prominence of the tendons and the 
intervening furrows, may become diminished or effaced. The normal 
displaceability and elasticity of the skin gives way to a more hide-like or 
leathery-like texture, whilst the cutis itself, need not necessarily appear to 
be thickened. The toes in the territories that have suffered most marked 
circulatory impoverishment may be enlarged, waxy in appearance, devoid 
of wrinkles or furrows, and filled out as it were, in a manner that does not 
yield to pressure, as does edema. 

Alterations in the nails may be the sequence of trophic lesions in their 
immediate neighborhood, as in the healed ulcerative lesions; or the nails— 
especially of the fingers (Chap. LIX, p. 298) may become distorted, lifted off 
the matrix and opaque, whilst the matrix becomes white, the cuticle retracting 
so as to leave an exaggerated, enlarged, yellow white and dirty looking lunula. 

Fissures over the soles, between the toes, near the margin of the nails, in 
and near callouses, must not escape the watchful eye. For not only do these 
give pain, but they may extend much deeper than we would suppose at first 
glance, and further, may be but the harbingers of a serious menace 
to the integrity of the part. For out of these, infections and gangren¬ 
ous lesions are apt to develop. 

Atrophic changes of the skin are more often symptomatic of the results of 
marked atherosclerotic disease than of thrombo-angiitis obliterans. How¬ 
ever, in that stage of chronic pseudophthisis or atrophy of the limb that occa¬ 
sionally belongs here; or in some of the pseudo scleroderma lesions, or in the 
vicinity of amputed limbs, striking atrophy is occasionally encountered. 

A peculiar mottling of the skin of the distal parts, especially over the 
digits seems to be the result of chronic circulatory disturbances. If one 
compares this mottling of the diseased with the normal foot, one can appre¬ 
ciate that it really represents an intensification of the normal venules, which, 
by virtue of stasis, b ecome permanently dilated. The mottling .is produced 
by streaks rather than by patches of discoloration and is brought out with 
greatest intensity when the limb is held up for purposes of eliciting ischemia. 
In some cases, hemorrhages take place with pigmentation, resulting in a 
permanent brownish discoloration. The skin is apt to be thin over such areas 
but when there is a combination of chronic enlargement of the toes, the 
general puifiness may be obscured by mottling. 

Atrophy of the leg, more rarely of the thigh, in varying degrees, is not 
uncommon where the popliteal and femoral arteries have become closed. 
This diminution of the girth of the calf is best appreciated with the patient 
in the prone position, when the contrast in the size of the calf muscles is 
noticeable. 


T H ROM BO-A NGIITIS OBLITERANS—ISCHEMIA 


237 


CHAPTER XLV 

THROMBO- ANGIITIS OBLITERANS—ISCHEMIA 

Ischemia, blanching or whiteness of the peripheral parts, usually affects 
the toes, feet and legs, and more infrequently is distributed over the 
corresponding portions of the upper extremities. It may be considered as 
of two distinct varieties, each having an essentially different cause. Irrespec¬ 
tive of the source of immediate inducement, such as external or even internal 
exciting factors, the blanching in thrombo-angiitis obliterans seems to have 
two absolutely diverse modes of creation, so that we may speak of: 

I. Mechanical or hydrostatic ischemia. 

II. Vasomotor ischemia. 


I. MECHANICAL OR HYDROSTATIC ISCHEMIA 


Pallor or ischemia is evoked by elevating the limb from the pendent 
position to that extent which is incompatible with arterial influx into the vessels 
and capillaries oj the skin. With healthy arteries and adequate heart action 
the normal arterial vis a tergo is adequate to deliver blood into the most 
peripheral parts of the foot, that is, into the tips of the digits, and lend and 
conserve a pinkish normal blood tint in the distal skin areas. If in dorsal 
decubitus, the leg is raised to the vertical, any occlusive or obturating process 
in the chief arteries, makes such visible and customary color conserva¬ 
tion impossible. Superadded to an abnormal diminution of blood supply 
in such a position is a certain degree of depletion and evacuation in the 
vascular system and one that conforms to the laws of gravity. In this sense, 
therefore, we may speak of mechanical or hydrostatic ischemia in obstruc¬ 
tive, occlusive, obturating or obliterating types of vascular disease of the 
extremities. 


Whilst vasomotor phenomena responsible for fugitive and transitory 
patches or even extensive areas of local syncope may be associated and 
confuse the clinicians’ concept of hydrostatic ischemia, a careful comparative 
estimate of the phenomena, as they appear under various conditions, in 
any case, will usually permit of definite differential recognition. A 
knowledge of the coincidental occurrence of the two blanching phenomena is 
a prerequisite for a comprehension, not only of thrombo-angiitis, but also 
of the vasomotor and trophic neurosis so frequently confounded with it. A 
few tests, and subjective or objective considerations should suffice to dis¬ 
tinguish the two types of ischemia. 

Mechanical or hydrostatic pallor should be studied in the following way: 
Relative to 


1. The situation of its appearance. 

2. The angle of elevation that brings it forth. 

3. The time that must elapse for its definite establishment. 

4. Its extent. 


5. The arc in which pallor persists. Its complement will be the residual 
angle to which lowering of the limb must continue, for the restitution of a 
normal or reactionary red color (Angle of Circulatory Sufficiency, Chap. 


238 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


6. The persistence of well localized areas of ischemia even after return 
and reaction have been established by descent of the limb; especially when 
the phenomenon can be reproduced in the same situation by subsequent 
preliminary tests of elevation and depression. 

From this summary it will be seen that the striking and distinctive feature 
of this form of ischemia, is its dependence on, and variation with position of the 
limb. By this it can at once be distinguished from the neurotic or vasomotor 
type. 

1. Situation of Its Appearance. —As the leg is elevated, pallor is seen to 
replace the usual rubor that pendency brings on. The toes and then the 
foot become abnormally pale, the veins flattened and depleted, the peripheral 
digits often evidencing patches of cyanosis that may persist throughout the 
period of elevation. The simultaneous blanching of the toes and foot, 
possibly coupled with arteriovenous depletion throughout the leg, suggests 
arterial occlusion of greater degree or greater inadequacy of the collateral 
circulatory paths. Occasionally by irregular sequence, the pallor of the 
foot may antecede that of the toes; one of these, usually the big toe, may 
remain cyanotic and even the other toes may evidence a mottling or redness 
due to intracutaneous hemorrhages; or, other variations may be noted. 

Certain adventitious factors contribute to the difficulties attending the 
correct estimate of the appearance of pallor. Thus, a continued cyanosis, 
particularly in cold weather, or transitory vasomotor irritants exciting even 
blanching in the pendent position, must not be confused with hydrostatic 
conditions. For it is the latter alone that are of value in diagnosis of the 
malady and in the appraisement of the degree of vascular obliteration. We 
must await, therefore, altered circumstances, give aid by establishing a proper 
environmental temperature state, and allow for psychic repose before making 
a test for the appearance of ischemia. 

Pallor on elevation may affect only a few of the toes at the outset (one, 
two or more); or, there may be successive blanching of one after another 
without orderly sequence, the intensive cyanosis and rubor being recalcitrant 
and abolished with difficulty through action of gravity. 

An extraordinary degree of blanching of a single toe, associated with 
chronic cyanosis in the pendent position, warrants the suspicion that gangrene 
or trophic disorder is imminent. 

When the feet are very cold and apt to be cyanotic, as often occurs in 
winter, a combination of rubor and cyanosis permits only very slow and 
patchy replacement of color by yellowish white areas over the toes, until a 
considerable time has elapsed. 

2. The Angle of Elevation That Produces It.— Theoretically this should be 
but slightly greater than that at which reactionary rubor is called forth. 
In truth, however, the two do not correspond, since, for a given time a 
distinctly greater elevation is required to establish pallor, than the minimum 
angle at which it still persists. Thus, if we have to elevate a limb to 170° 
to evoke ischemia, we may find that pallor still exists when the leg is depressed 
through a considerably larger arc than io°. In a severe case with marked 
circulatory impairment, it is not unusual to find ischemia established at 135 0 
or less, and continue for an indefinite time in the horizontal (90°). In 
other instances pallor ensues almost at once on elevation to the bed level 
(90° or horizontal). 

When the degree of inducible blanching is doubtful or slight, a good 
comparative estimate of the two limbs may be attained by resorting to one of 
the following two methods; to, 


TH ROM BO-A NGIITIS OB LI TERA NS—ISCHEMIA 


239 


(a) The repeated elevation and descension of the limb, two, three times or 
oftener, with possibly, coincident production thereby of a reactionary rubor 
during pendency, may evoke an ischemia otherwise concealed; or 

( b ) Careful observation of plantar aspect of the foot as it is raised and held 
up, in varying positions with the patient prone and the leg flexed through 
varying angles. Frequently distinct pallor is noticeable with the leg vertical 
( 9 °°). 

3. Time Interval for Its Establishment. —Employing approximately the 
vertical (180° elevation) as a routine test, this generalization is acceptable, 
that the more rapid the onset and completion of ischemia, the greater the 
extent of vascular obturation. We must view both dorsal and plantar 
surfaces of the foot, and even the leg with careful scrutiny and with adequate 
but not too glaring illumination, for a dependable appraisal of this valuable 
sign. 

Where chronic cyanosis has set in, it may completely nullify the quanti¬ 
tative value of this proof of circulatory disturbance. Under such circum¬ 
stances we are, however, usually dealing with severe and extensive forms of 
vascular obliteration. 

Hemorrhagic infiltration of the skin and subcutaneous tissues, as also 
pigmented areas, the products of previous disturbances, may give confusing 
mixtures of colors that vitiate the general pallor that is to be expected. 

A comparison of color phenomena displayed in the two legs will give 
valuable information as to prognosis, since the more extensive involvement is 
usually distinguished by more rapid evolution and greater distribution of the 
ischemia. 

4. Extent of Ischemia. —Usually, by virtue of the advanced condition 
of vascular obliteration existing even at the first consultation, pallor on 
elevation is apt to involve the whole of the foot and more or less of the distal 
third, half or even two thirds, of the leg. Occasionally one toe alone, or 
several of the toes will show definite blanching whilst an appreciable color 
change is difficult to elicit elsewhere. It may, however, be persistently con¬ 
fined to the same number of toes, this localization lasting for a variable time 
yielding to more extensive blanching as the inadequacy of collateral, and 
implication of additional arteries advances. 

Where ischemia is well established in the horizontal position it is usually 
limited in extent, rarely occupying a greater territory than the whole foot, 
often restricted to one half of the foot or to some of the toes. 

Careful continued and repeated observation over weeks and months may 
reveal the striking fact, that ischemia may disappear, sometimes together 
with the rubor and the trophic disturbances. These are the cases of arrested 
symptoms and so-called “cures.” In some of the quiescent cases all other 
signs (except lack of pulsations) may disappear, but ischemia on elevation 
will endure for years. 

Per contra it is more usual to witness the reverse, namely, gradual increas¬ 
ing intensity of blanching associated with progressiveness in the other 
phenomena. 

It is not uncommon to find seemingly inexplicable vagaries in the location 
and intensity of the white patches, and also coincident lividity. The signifi¬ 
cance may be better appreciated from a rehearsal of an instance such as the 
following. 

In case, M. S., after elevation of the leg, the pallor is admixed with patches of cyanosis 
that almost look hemorrhagic. These are distributed over the big toes, being most promi¬ 
nent over their plantar aspects. Complete ischemia is very hard to elicit because of the 


240 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


persisting cyanotic areas although some look hemorrhagic. They can be proven to be foci 
of stasis because blood can be dislodged by pressure converting them into pallid spots. 
Not dissimilar lividity accompanies localities of imminent gangrene; but such do not become 
pale. 

Even after the induction of reactionary rubor which may begin over the ankle and spread 
slowly over the dorsum and plantar aspects of the foot, a larger or smaller area of pallor 
may remain either over the dorsum or the toes. Suddenly rubor may loom up in a distal 
part, leaving here and there a mottling of white. The tip of the big toe may remain white 
the longest, retaining a slight livid hue. Such a phenomenon is evidence of the poor circu¬ 
lation in the big toe, especially when it is last to regain a pinkish tint. When it becomes 
necessary to bring the leg to the pendent position to effect the latter, a valuable hint as to 
the gravity of the prognosis in this locality is at hand. 

5. Arc or Angle of Persistent Ischemia. —Since this is the complement of 

the angle of circulatory sufficiency the phenomenon of blanching and its 
behavior on depressing the leg after prior ascent, will merely be touched upon 
here. Generally speaking, the greater the arc within which ischemia con¬ 
tinues to remain in evidence the more extensive the arterial occlusion. A 
limb that remains blanched in situations between 180° (vertical) and 70° 
(20° below the horizontal) is one whose circulation is badly compromised. 
More frequently reactionary rubor is perceptible before descent reaches the 
horizontal. Although this angle cannot be estimated with mathematical 
accuracy, an approximate appraisal will suffice as a good working guide. 
This absence of precise delimitation between disappearance of ischefnia and 
reentrance of rubor, is responsible for the inaccuracy of the test. Thus pallor 
over certain toes or even part of the foot may be difficult to dislodge and on the 
other hand, rubor may develop in patches that alternate with recalcitrant 
areas of pallor. If sufficient time be allowed to elapse, however, the reaction¬ 
ary rubor will finally disappear and cause every vestige of ischemia to vanish. 

6. The Obstinate Areas of Pallor. —When one or more toes, or areas, on 
repeated examination fail to become red when the test for reactionary rubor 
is made, and when such well localized spots of sanguinous depletion are visible 
even at the horizontal or at an angle of greater depression, we then have 
valuable evidence of marked local deficiency of circulation. Such areas are 
apt to be the seat of gangrene, at no remote date. When there is a history of 
spontaneous blanching in the same locality, or such discoloration after a walk 
in the cold, or when the situation of the pain coincides with the distribution 
of the pallor, strong corroborative testimony of impending gangrene or trophic 
disorder is in our possession. 


II. VASOMOTOR ISCHEMIA IN THROMBO-ANGIITIS OBLITERANS 

Since local syncope is discussed elsewhere, and many of its striking features 
defined in detail, it will be merely necessary here to allude to that perplexing 
association of pallor of neurotic origin, with the multiform color manifesta¬ 
tions of mechanical or hydrostatic causation. For, even in organic maladies 
of the vessels where objective signs are eminently due to vascular obliteration, 
a coincident display of vasomotor phenomena may create a confusing clinical 
picture. A narration of the clinical manifestations alone will be attempted, 
since the explanations of such occurrences are still too vague and unsatisfactory 
to warrant argumentation. Suffice it to say here, that the implication of the 
nerves, and the perivascular chronic inflammatory process so noteworthy in 
thrombo-angiitis obliterans, may be responsible in part at least, for a loss of 
normal vasomotor stability. 


TH ROM BO- A NGIITIS OB LIT ERA NS—ISCHEMIA 


241 


To what extent metabolites, or a vicarious functional implication of the 
autonomic action of the capillaries and arterioles is responsible for these 
phenomena, future investigation may help to clarify. 1 Furthermore, it 
has been the contention of a number of physiologists, that a vasomotor 
constriction may be the sequence of ischemia alone whenever a part is arti¬ 
ficially depleted of blood, just as a hyperemia is incident upon subsequent 
filling of the emptied vascular channels. In conformity with this hypothesis, 
a neurogenic reflex can play a role whenever there is abnormal anemia or 
plethora. 

Too much emphasis cannot be laid on the fact, however, that most of the 
objective symptoms regarded and described by many authors as of neurotic 
foundation, are merely hydrostatic and compensatory phenomena; although, 
it is true, independent vasomotor disturbances may be concomitant and clini¬ 
cally mystifying in appearance. 

Vasomotor ischemia in thrombo-angiitis obliterans seems to be especially 
influenced by cold and exertion; it is independent of posture, since it may occur 
in the horizontal and pendent positions as well as in the elevated. It differs, 
too, from hydrostatic and mechanical ischemia in that it may come on with¬ 
out apparent cause, alternate with rubor, and offer thus a variegated display 
of color tints that stamps the phenomenon as the result of a neurotic agency. 

Especially notable are such manifestations when they occur in cases of 
thrombo-angiitis obliterans in which other objective pathognomonic signs 
have not developed sufficiently to warrant a positive diagnosis. 

Since these manifestations are frequently more pronounced in the early 
stages of thrombo-angiitis obliterans than later in the course of the malady, 
diagnostic uncertainty must necessarily exist in the minds of those not thor¬ 
oughly conversant with the relative significance of the two types of ischemia. 
An interesting example of the independent occurrence of the two varieties of 
pallor may be worthy of consideration. 

Vasomotor Phenomena in Only One Leg. Usual Clinical Course of Organic Vascular 
Disease in Both. —H. R. presented simultaneously striking vasomotor signs in the right, and 
typical objective symptoms of thrombo-angiitis obliterans in the left. Later, whilst under 
observation, the vasomotor phenomena gradually disappeared, the disease taking its usual 
course in both extremities. 

Thrombo-angiitis Obliterans Symptoms in the Left Leg, December, i, 1908.—On taking 
off the shoe the left foot appears markedly red; the dorsalis pedis, posterior tibial and popli¬ 
teal arteries are pulseless; there is marked ischemia on elevation. 

Vasomotor Signs in the Right. —At the same time the right foot was found blanched in 
the pendent posture, cold, and patches of cyanosis appeared. All the vessels pulsate. 

On December 24, the picture was still more striking. At this moment the progressive¬ 
ness of the malady was noted by the disappearance of both posterior tibial and dorsalis pedis 
pulses on the right. 

Upon taking off the shoes and stockings and examining the lower extremities, the differ¬ 
ence in color between the left and right foot is remarkable. On the left the swollen and 
enlarged toes are of a deep red color, the hue extending up the dorsum of the foot is most 
intense on the inner side of the foot and fades off gradually towards the ankle. The right 
foot is of a peculiar yellowish white color, the toes are most markedly blanched and are 
distinctly smaller than on the left foot. {Angiospastic pallor of the right foot in pendent 
position .) 

After the feet hang down for about five minutes their color changes. The color of the 
left becomes admixed with a blue tint, which gives a livid appearance to the foot, the purple 
color being particularly striking over the toes; here and there bright scarlet patches stand 
out prominently between areas of cyanosis. The right foot still retaining its more slender 
appearance has become cyanotic, the distal phalanges being of a deep dusky purple unmixed 
with any tinge of red, and the rest of the foot also shows a cyanotic hue but somewhat toned 
by a pale ashy skin, which shines through in many places. After the right foot has 

1 See Chap. VII concerning the independent action of capillaries and arterioles. 

16 


242 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


remained in the horizontal position for about five minutes, a little of the normal color 
appears over the fourth and fifth toes, but the first three toes are still quite blue. 

After cyanosis had set in, however, ischemia dependent on elevation could regularly be 
demonstrated in the right foot—this being the noteworthy diagnostic point in favor of thrombo¬ 
angiitis obliterans. 

March i, 1909, amputation of the left leg. In November, 1908, the angiospastic condi¬ 
tion in the right foot had disappeared, the popliteal artery no longer pulsated, the disease 
evidently making progress. 

January, 1919, amputation of the right leg; specimen showing typical lesions of thrombo¬ 
angiitis obliterans. 

Conclusions. —A period of vasomotor disturbances as predominating objective sign 
in the right leg; rapid development of thrombo-angiitis obliterans in the left with amputa¬ 
tion; disappearance of vasomotor phenomena in right, followed by usual symptoms of 
thrombo-angiitis obliterans. 

A further discussion of this type of blanching is relegated to the chapter on 
Vasomotor Symptoms in Thrombo-angiitis Obliterans. 

Ischemia, an Index of Circulation. —We have elsewhere alluded to the 
value of the angle of circulatory sufficiency as an approximate clinical 
measure of the circulatory condition; and also to the fact that the obstructive 
effects vary in inverse proportion to the size of the angle (above the 
horizontal) through which the limb must be elevated before pallor is estab¬ 
lished. In acute exacerbation of any of the organic types of vascular occlu¬ 
sion, when either by virtue of extension of the disease per se, or through 
superadded accretion, bland or mechanical thrombosis, new vascular territories 
become involved; these methods of circulatory appraisal become even more 
reliable and valuable—for compensatory collateral paths (an otherwise 
misleading factor) have not as yet become adequately established. 

If cases of atherosclerotic disease of the arteries can be observed during 
and after attacks of thrombosis, we can note subsequent improvement of the 
circulation, not only by the usual signs, but also by estimating the altitude to 
which elevation of the leg is necessary for the advent of the first signs of 
blanching. Very frequently, ischemia is present even in the horizontal posi¬ 
tion, shortly after thrombosis or embolism. As the limb improves, the leg 
must be raised higher and higher to elicit the ischemia. Early in the clinical 
course of the embolic and thrombotic cases, a production of the blanching is 
easy, for then a very slight raising of the limb above the horizontal is apt to 
produce it. 

These observations apply also to other forms of organic vascular maladies 
where obstructive conditions of the circulatory channels are at hand. 


CHAPTER XLVI 

THROMBO -ANGIITIS OBLITERANS—ERYTHROMELIA 1 

Erythromelia? Rubor , Hyperemia. —We may divide the rubor accompany- 
ing this affection into (1) inflammatory, (2) non-inflammatory or intrinsic 
rubor, and (3) the vasomotor. 

Types of Rubor— 1. The inflammatory rubor or hyperemia hardly requires 
comment, in that it is associated with inflammatory processes, differing only 
in so far from the reactive redness of the normal, that it is apt to be less 

. 1 P° r other interpretations of erythromelia in the light of the findings of capillary 
microscopy, the reader is referred to Chap. CVII. 

2 This term must not be confounded with that of “ erythromelie ” proposed by Pick for 
the disease, Idiopathic Atrophy of the Skin (see Chap. Scleroderma). 



TII ROM BO-A NGIITIS OBLITERA NS—ERYTHROM ELIA 


243 


intense in the neighborhood of trophic lesions than we would expect with 
healthy vessels. Edema and lymphangitis are often coexistent lesions. 

2. The intrinsic rubor or “ erythromelia” (as the author has termed it) 
seems to be due to compensatory dilatation of the superficial capillaries. 
This manifestation has led to much confusion in the differential diagnosis 
between erythromelalgia and thrombo-angiitis obliterans. It is a red blush 
of varying degree or intensity, that usually begins in one of the toes (big toe 
especially) and extends over all the toes for a variable distance up the dorsum 
of the foot. It may be so slight as to necessitate comparative exposure of 
both feet for its detection, or so marked as to partake of a crimson or Vermil¬ 
lion hue. Its appearance is enhanced in intensity and expedited in develop¬ 
ing by allowing the limb to hang down, the color increasing gradually until it 
attains its maximum, when a slightly cyanotic tint is wont to be admixed, 
whilst the dorsal veins of the foot attain their maximum prominence. 

When rubor is present in any position between the horizontal and the 
pendent, when it is manifest at room temperature in these postures, we term 
it chronic rubor or erythromelia in contradistinction to that rubor which is 
induced after preliminary elevation of the limb. The advisability of making 
so subtle a distinction will be made clear when the importance of the two 
manifestations in diagnosis will be discussed. 

Chronic rubor or erythromelia is an inherent, characteristic and unmistak¬ 
able stigma of defective circulation in the deeper vessels and its chronicity 
and dependence upon posture of the limb should at once differentiate it from 
the rubor of vasomotor origin. It is not only influenced in intensity as the limb 
is elevated or depressed, but suffers change secondarily through any circu¬ 
latory alteration that may be transmitted to the deeper vascular channels. 
As elevation of the limb empties the deeper channels, so also, will blood be 
drawn from the superficial parts, both through evacuation by gravity, as 
well as by diminution of the supply. Variations in erythromelia upon 
changes of position are greatest where the deep vessels are most extensively 
diseased. 

Mere elevation to the horizontal may decrease the redness considerably, 
while lifting the limb towards the vertical causes its complete disappearance. 

The position (angle or level) at which the hyperemic manifestations 
appear is subject to variation. Sometimes rubor is apparent with the leg 
elevated slightly above the horizontal, at the horizontal, or below this level. 
It is evident that these types must correspond to different degrees of circu¬ 
latory impairment, the vascular obliteration being doubtless most extensive 
in the last type, or, per contra, the collaterals are least adequate. 

Although erythromelia is a very constant symptom and usually appears 
at some time during the course of the disease, it may be continuously pres¬ 
ent in some, be absent in others, and in still other cases may persist for a 
long time, disappearing completely when the symptoms have abated or the 
limb is in a “ cured state. ” In two cases (S. and J. R.) erythromelia remained 
for a considerable length of time, and then completely disappeared when 
the limb was free from symptoms. 

Reactionary or Induced Erythromelia. —With the limb held high for a time, 
subsequent pendency is regularly followed by a reactionary or induced rubor 
of much greater intensity. This phenomenon is closely analogous to the 
hyperemic reaction that follows the application and removal of a constricting 
bandage to an extremity. Since ischemia must precede its production, its 
demonstrability indicates that a state of arterial occlusion or impaired circula¬ 
tion must exist. For, without occluded vessels, the mere elevation of the limb 


244 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


is ineffective in causing the requisite blanching. T he importance of reactionary 
or induced rubor in the recognition of obturated deep vessels can thus read¬ 
ily be realized. In a routine examination of cases of suspected arterial 
occlusion, the contingency of appreciably altering the degree of rubor by a pre¬ 
liminary lifting of the limb must be considered. And it is always advis¬ 
able, therefore, in order to gain a correct estimate of this symptom, to 
examine the extremity first, in the dependent position (as the patient walks 
into the office), second, in the horizontal position, third, in the elevated, 
and finally, again in the pendent, when the reactionary or induced rubor will 
be viewed. 

Partly by reason of thermal constricting influences (vasomotor), 
and partly for other reasons, it is not always feasible to demonstrate a very 
noticeable reaction. In such cases, the procedure of elevating and depressing 
the limb must be repeated two or more times, in such^a manner as to permit 
ischemia of one minute duration to be followed by a reactionary period of 
about three minutes or more. We will not infrequently be rewarded by thus 
evoking a most exquisite rubor that seemingly could not be elicited at all. 

Not only is this a valuable diagnostic sign in indicating the existence of 
arterial occlusion, but may be utilized to differentiate between the relative 
activity and extent of the obliterative process in the two limbs. Further¬ 
more, it may be exhibited at a time when the chronic rubor is so slight as to 
be doubtful. Fine distinctions, such as a color reaction in the horizontal 
position in one limb, and in the position of complete pendency in the other, 
with appearance over the leg before it reaches the toes and foot, are amongst 
the variations encountered. 

Reactionary erythromelia is frequently of value in the diagnosis of those 
cases, in which, for a long time, there are no symptoms other than pulseless 
vessels (possibly only the dorsalis pedis), and pain. In these, fairly marked 
induced rubor may be present long before the characteristic chronic rubor 
develops. 

Thus, in one case H. F., absent dorsalis pedis and posterior tibial pulses, with reactionary 
erythromelia were the only signs of thrombo-angiitis obliterans. Ischemia was doubtful. 
Later on Qune n, 1910), a slight chronic erythromelia appeared. Under our own eyes 
erythromelia developed, but for a long time we had to have recourse to the reactionary 
rubor in making the diagnosis. 

A careful scrutiny of the color changes accompanying the induced rubor 
may lead to conclusions of diagnostic and prognostic importance. 

With the advent of the reactionary eyrthromelia in certain cases, it is 
very interesting to note how certain portions of the foot will remain white 
longer than others. By digital compression of the hyperemic areas, the 
rapidity of hyperemic return will show differences of circulatory activity in 
various toes. 

To cite an example:—In the case S. L., all of the toes and an inch and a half of the 
dorsum remained white for 3 or 4 minutes, although the rest of the dorsum became very 
red. The return of blood into the toes was not simultaneous, but the fourth and fifth 
showed rubor, whereas the first, second and third remained white. Patches of white also 
persisted over the dorsum. The big toe of the right foot remained white for a long time, and 
the reactionary erythromelia existed much longer in the foot that was markedly affected 
than in the other in which the symptoms were slight. 

Other variable phenomena associated with induced rubor are of no mean 
value in the acquisition of a general concept of the pathologic conditions at 
hand. Evidences of inadequate circulation are notably enhanced by the 


TH ROM BO-A NGIITIS OBLITERA NS—ER Y TH ROM ELI A 


245 


induction of this type of rubor. The observations in the following case 
will illustrate. 

In the case, M. S., the reactionary erythromelia begins to appear over the left ankle 
extending slowly over the dorsum and plantar aspects, leaving a large and small area of 
pallor over the dorsum and the toes for some time. Then it looms up at a more distal part, 
leaving here and there a mottling of white. Remarkable, however, is the fact that the 
tip of the big toe remains white longest, and with it there is an admixture of cyanosis. A 
similar condition obtains in the right leg but not so marked. It is necessary to depress the 
foot to obtain rubor of the big toe. 

In short, here are phenomena expressive of the poor circulation in the big toe, since it is 
the last to regain its circulation; and here is exemplification of the value of inducing rubor 
to confirm signs that might be misinterpreted as of vasomotor origin. For, indeed, local¬ 
ized syncope may occur even in organic obstructive arterial affections. 

Cold and vasoconstriction from other causes may temporarily prevent 
the demonstration of both chronic and induced rubor. So it may be neces¬ 
sary either to warm the extremities affected or to artificially further the 
dilatation of the superficial vessels by repeated changes of posture. The 
latter is done by elevating the limb for i minute, so as to produce ischemia, 
then to depress it for 2 minutes. Several changes of position will eventually 
evoke a reactionary rubor that may be otherwise indefinitely postponed by 
reason of vasoconstricting influences. 

Duration of the Chronic Rubor .—When the postural treatment of the 
author is successful in dispelling most of the symptoms, then we often note a 
disappearance of the chronic erythromelia. Such disappearance of the 
chronic rubor with a slight reactionary rubor, however, can be elicited even 
when erythromelia is absent. 

In short, the chronic rubor disappears before the reactionary. The 
following case will exemplify. 

J. K., 37 years of age, November 24, 1920, presented the typical history and physical 
appearance of thrombo-angiitis obliterans involving both lower extremities, and the devel¬ 
opment of an ulcer of the small toe, and another between the second and third toes of the 
left foot. These have not healed. 

A deep ulcerating fissure at the base of the little toe is observed, the foot in a state of 
chronic rubor, the big toe slightly tumefied, and an ulcer over the small toe. The dorsalis 
pedis and posterior tibial pulses are not perceptible. The postural treatment was 
prescribed. 

April 14, 1921, still marked rubor of the left leg and absent pulses of the right are 
recorded. 

October 24, 1921.—The chronic rubor has disappeared completely, but the dorsalis 
pedis and posterior tibial arteries are still pulseless; postural treatment continued. 

October 16, 1922.—Both feet have a normal appearance; disappearance of the chronic 
rubor, but reactionary rubor can still be elicited, but of slight degree. His symptoms have 
almost disappeared, demonstrating (1) the value of the postural treatment; (2) the dis¬ 
appearance of the chronic rubor; and (3) the persistence of the reactionary erythromelia. 

A similar change in the character of the rubor is not uncommonly noted 
in the upper extremities, where, however, the restitution to a normal appear¬ 
ance of the hand is more striking than in the case of the lower extremities. 
The reactionary rubor persists long after the chronic rubor has disappeared. 1 

3. Vasomotor rubor may enhance an existing intrinsic or chronic rubor, 
but more frequently is a patchy hyperemia of small extent interspersed with 
areas of pallor. It may be reactive and follow that abnormal pallor of the 
foot which is induced by cold. More data on vasomotor phenomena will 
be given in Chap. LIV. 

Significance of Rubor. —Whilst we do not expect a formal and definite 
reciprocation between the dilatation of the superficial vessels and the quantita- 

1 See p. 298, case R. L. 


246 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


tive organic inroads on the deep circulatory channels, a partly abortive and 
partly successful attempt is nevertheless made here by Nature to improve 
the delivery of blood. This is accomplished, probably, by inhibition of 
vasoconstrictor stimuli (or stimulation of vasodilators); but just how, it is 
difficult to determine. In contrast with the establishment of the functionally 
more potent deep collaterals (Chap. XII), this generalized tegumental 
and subcutaneous vascular ectasia is but a vicarious attempt. Reasoning 
a posteriori from the beneficial effects of the author’s postural treatment , 1 it 
must be regarded as an index or partial measure of an accompanying enhance¬ 
ment of vascular girth and patency in the deeper arteries. 

In the “postural” procedure we call forth hyperemia by an artificial 
sequence of changing positions. Knowing that induced rubor will follow 
the preliminary blanching produced by elevation, we posit, therefore, that 
such reactionary rubor—which is but a heightened erythromelia, and only 
the external visible characteristics of which are perceived—is valuable, not 
only through its amelioration of the skin circulation, but also because it may 
be, and probably is, associated with similar angiectatic or expansive phe¬ 
nomena in the muscular and other deep arterial branches. 

A number of interesting phenomena attest the heightened vasomotor 
instability of the vessels supplying the skin, when either chronic, induced 
or both types of rubor become visible. Thus, the occurrence of irregularly 
outlined and evanescent areas of pallor, interspersed amongst the general 
redness that is evoked by elevating and then depressing the limb, is a mani¬ 
festation of more severe impairment of circulation in the limited ischemic 
area, or merely significant of a prolonged angiospasm. Setting aside the 
former type which is evidence of chronically impoverished circulation for 
consideration elsewhere , 2 let us appraise the importance of the observations 
from which the vasomotor nature of the latter has been deduced. 

We have already noted that when induced rubor is elicited, certain fugitive 
spots or areas of pallor will outlast the general ischemic color, but will, after 
a variable time, also be replaced by redness. What causes these pallid spots? 
Why is the blanching so transitory? 

Upon reflection it will be admitted that but three explanations are 
applicable. Either there is a permanent narrowing of the arterioles and 
capillaries of these parts that is more intensive than in the surrounding area; 
or, the vis a ter go is insufficient to fill these as quickly as elsewhere; or a 
vasoconstriction is present, which outlasts any such phenomena that may 
have been present in the adjoining parts. Of these three different views, 
the last seems to be the most plausible explanation. 

Noteworthy and significant is the fact that the transitory type of persist¬ 
ing ischemia does not affect exactly the same areas on all occasions, but 
even during the same interview and examination, repeated tests for induced 
erythromelia may bring forth varied pictures. Certainly, therefore, an 
organic cause cannot be ascribed to the phenomenon. 

Furthermore, it is not the most distant parts that are the seat of it, the 
dorsum of the foot at points considerably removed from the tips of the toes 
evincing it as frequently as the most peripheral parts. Therefore, an incom¬ 
petent propelling force from behind is also not responsible. The bizarre 
colored appearance should , therefore , be attributed to an unstable nervous 
mechanism. 


1 Postural treatment is described on p. 380. 

2 See Chap. XLV. 


TH ROM BO-A NGIITIS OB LI TERA NS—ER Y TH ROM ELI A 


247 


We believe that immediately on elevation of the leg and particularly 
through prolongation of this position an arterial constriction may occur, as a 
necessary functional and compensatory action. For, the diminished arterial 
supply through the scant vascular channels and the reduced vis a tergo in 
the distal parts, accounts for collapse of vessels when blood has to flow up 
hill. A vasomotor constricting influence is the necessary sequence, though 
its occurrence cannot be predicated for all cases. Depressing the limb, since 
it causes a sudden inflow, should normally evoke a relaxation of the contracted 
vessels. In fact this occurs in the areas that are the seat of reactionary rubor. 
Pallid zones then, are those in which such vasodilatation is temporarily in 
abeyance. 

Where more or less permanent, identically situated ischemia , oft attended 
with cyanosis, is a feature in the peripheral part of a digit, or other distal part 
of the foot, organic vascular occlusion is usually the cause. 

Explanation of Erythromelia.—An attempt was made by the author to 
investigate clinically whether the dilatation of the capillaries and arterioles 
producing chronic rubor was of paralytic nature. The induction of derma- 
tographia suggests that in most cases, a true palsy of the capillary activity 
does not exist. The observation that cases lose their chronic rubor when 
they improve after the postural treatment, also speaks in favor of this 
conclusion. 

If we cause the red type of dermatographia (dermatographia rubra) in a 
foot that is in a state of chronic rubor, and subsequently bring about ischemia 
thereof by elevation, blanching of all of the skin is produced, the reacting 
streaks showing slightly as very faint bluish red lines, or not at all. On 
subsequent depression of the foot, it will be seen that the reactionary rubor 
may appear first in the streaks of dermatographia and later in the immediately 
surrounding areas. This would seem to warrant the conclusion that there 
has been produced a distinct comparative alteration in the tone of the capil¬ 
laries of the scratched areas, one that temporarily puts these into a state of 
dilatation, whilst the surrounding parts yield to the reflexes gradually and 
show belated dilatation in the pendent position of the limb. If complete 
palsy of the capillaries were present, no such difference in time of response 
should exist. 

Whether the delayed rubor indicates belated reflex dilatation or slow 
chemical response on the part of the capillaries, is an open question. At any 
rate, the conclusion is warranted that the finer vessels are still able to respond, 
and are not wholly inert and paralytic. 

Can we satisfactorily account for the striking rubor so characteristic of 
this affection, and of other obliterative arterial diseases? To state that it 
is a compensatory phenomenon is merely an expression of a teleological view, 
and an assignation of a distinctive attribute to the phenomenon. We can 
obtain illuminating information on its modus operandi, however, by inten¬ 
sive clinical and anatomical studies. From such, the author would offer 
the following explanation. 

We assume that with the exclusion of the normal major circulatory 
channels, although there is a generally diminished pressure, a relatively 
larger amount of blood tends to remain in the superficial arterioles and 
capillaries. This blood arrives through devious channels by circuitous 
routes, and by virtue of the diminished vis a tergo must needs remain longer 
in both arterioles and venules. In short, a sluggish circulation with stasis 
is the result—an inference that receives confirmation in the fact that the 


248 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


“expression test” (compression of the skin) always indicates a tardy return 
of blood into the integument. 

Does not this stasis in the arterioles and capillaries exert an effect which 
impresses itself upon, and evokes a response in the vasomotor innervation? 
We must answer in the affirmative. For, although anatomical alterations 
in the nerves accompanying the arteries (perineuritis) are concomitant lesions 
of thrombo-angiitis obliterans, these alone cannot be responsible; this, because 
rubor occasionally comes on rapidly after a sudden accession of thrombosis 
in arteriosclerotic cases, where' no perineural changes have been found. 
Erythromelia may be of rapid advent , signalize , and be synchronous with other 
evidences of an attack of acute thrombosis. In such , a neuro-anatomical and 
pathological causal basis can be excluded , and we must expect alterations in 
functional innervation as the creative grounds for the phenomenon. 

With the limb pendent, the constant stasis in the arterioles and venules 
then—whose existence is adequately corroborated by the color changes 
elsewhere described—may be regarded as influential in producing a state of 
chronic vasodilatation with partial exhaustion of the vasocontracting 
mechanism. That complete paralysis of the constrictor power does not 
occur, is proven by the occasional local syncope that goes with, and alter¬ 
nates with rubor in certain cases, and by the circumscribed and limited 
areas of pallor that outlast the generalized rubor, when the test for ischemia 
and induced erythromelia is carried out, and by the response to dermato- 
graphia occasionally elicited. 

In short, we postulate a maladjustment, malfunction and instability of the 
vasomotor mechanism, as the result of continued disturbance in the normal 
intravascular pressure. What is more likely than relaxation of the normal 
arterial tonus when the small vessels have lost the aid of the usual vis a 
ter go in the propulsion of blood through the tissue and back through the veins? 
Their muscular mechanism, just as in other viscera, may suffer; and they 
may lapse into a state of chronic dilatation, which we have elsewhere regarded 
as compensatory. In most instances however, their contractility is at least 
partially conserved. 

In erythromelia we presuppose an inhibition of the vasoconstrictor 
impulses, incited, accompanied and aided by hydrostatic conditions. In the 
usual ischemia on elevation or even in the horizontal position, we are dealing 
merely with a hydrostatic phenomena, one of pure depletion; although (as 
has been elsewhere pointed out) subsequent vasomotor contractions may 
supervene, and prevent for a time at least a rapid refilling of the vessels when 
the proper conditions of gravity (pendent position) are again restored 
(neurogenic ischemic reflex). 

In consonance with this conception, we predicate a division of the vaso¬ 
motor phenomena into two types:—First, that of central origin (as in 
Raynaud’s disease, erythromelalgia and the other vasomotor and trophic 
neuroses), and secondly, an essentially peripheral form (thrombo-angiitis 
obliterans, arteriosclerosis, and the other obstructive arterial diseases). 
Whilst the deranging nerve impulses in the neurotic type emanate primarily 
from the central nervous system, the aberrant vasomotor responses in the 
organic vascular processes, owe their origin to abnormal impulses from the 
periphery. Although this view is acceptable as applying generally, it must 
be qualified in so far as it does not imply that centripetal stimuli play no role 
in inciting the unstable nerve mechanism of the vasomotor neurotic type, nor 
that emotional, and other central agencies may be altogether impotent in 


THROM BO-ANGIITIS OBLITERANS—ERYTHROM ELI A 


249 


the organic arterial maladies. A more complete exposition of this subject 
is to be found in Chap. LIV. 

. When we speak of compensatory dilatation, we unwittingly seem to 
inject a teleological interpretation into effects whose origin may be wholly 
passive. But for the student, such inferential thinking serves a good purpose 
in emphasizing certain objective and therapeutically adaptable phases of the 
phenomena; and, therefore, is wilfully allowed to be incorporated here. 

If we were to attempt an explanation based on mechanical or hydrostatic 
laws alone, we would err in not having taken into account the nerve mech¬ 
anism, the autonomic action of the capillaries themselves, 1 and the possible 
secondary paralytic and exhaustive influences occasioned by the unusual 
obstructive impairment of circulation. Taking these forces into considera¬ 
tion, it would seem that all do not participate to an equal degree, or else the 
varied pictures, with or without fleeting vasomotor phenomena could not be 
explained. 

A detailed discussion of the roles of the numerous motivating and 
determining elements is given in Chap. VII on Physiology of the Capillaries. 
Here, we need but summarize our theories that superficial arterioles and capil¬ 
laries may attain a more or less chronic state of dilatation as the result of 
the following causes. 

(1) Exhaustion of the vasoconstrictor mechanism of primarily mechanical 
origin. 

(2) Local action of metabolites or katabolic agents in a field of 
impoverished nutrition. 

(3) Action of specific toxins on the autonomic capillary regulatory func¬ 
tions with paralysis of these. 

1. The Exhaustion of the Vasoconstrictor Mechanism. —With more or 
less constant collapse of, or diminution in the size of the arterioles and 
capillaries, we would have to assume, according to the accepted views of 
physiologists, that a chronic increased tonus in these vessels must be the 
response. How long can this continue without yielding to that paralytic 
stage which would objectively find its expression in the clinical state of 
erythromelia? But that this cannot whooly account for the altered vascular 
girth is demonstrated by the clinical phenomenon that with existing rubor, 
vasomotor syncope, transitory, localized, fugitive, but nevertheless present, 
may occasionally be conspicuous. How then could we reconcile an exhaus¬ 
tive or paralytic state with one still capable of responding to a nerve mech¬ 
anism? 

Whilst seemingly diametrically opposed conditions, these are not so 
diverse as they would appear at first glance, for, firstly, the vasomotor syncope 
but rarely occurs when the hydrostatic factors are still at play, as in the 
pendent position, and secondly, such fugitive neuromuscular activity as 
angiospasm can be dispelled and actually exhausted by the clinical method 
of inducing rubor already described (reactionary or induced erythromelia). 

As for the first contention, we note that vasomotor syncope in the pendent 
position is more apt to occur in those cases in which the disease has affected 
but limited and shorter territories, as in the clinically early or little advanced 
case; namely, in those in which exhaustion may be but partial and the vessels 
are still amenable to nerve influences. And secondly, by passive exercises in 
which the dynamics of hydrostatic and gravity nature are summoned into play, 
an actual insufficiency and exhaustive state of the capillaries and arterioles can 


1 Vide, also Chaps. XIII and LXXXVII. 


250 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


be demonstrated. For, given that syncope of neurotic nature in thrombo¬ 
angiitis obliterans which but occasionally qualifies the picture,, its fleeting 
nature can be readily recognized in the case in which the changing position 
of the limb may cause it to disappear. 

Nor must we interpret the absence of rubor in the horizontal position as an 
argument in favor of retained vasoconstricting powers. For, in such position, 
the force of the circulatory stream may be inadequate to force the blood 
through the collaterals and into the capillaries. Unfortunately, the effects 
of gravity must sometimes be called to aid in the production of rubor, so that 
an additional mechanical factor is injected. 

2. In consonance with the work of recent investigators, we must take into 
account that the products of local metabolism are believed to be a potent 
factor in producing dilatation of the smallest vessels. Are not. metabolites 
present in increased abundance in territories so badly nourished? Just 
what part is played by the chemical influences is still a matter of conjecture. 
That a vicious circle may be produced in areas (toes) that are in imminent 
danger of gangrene, seems more than likely, for that stasis occurs is clinically 
often demonstrable. 

Perhaps this excessive stasis that leads to cyanosis is furthered by the 
dilated condition of the capillaries. 

Whilst it may seem paradoxical to recognize the possibility of chronic 
dilatation of capillaries and venules, and to question the likelihood of a con¬ 
tinued state of tonicity without exhaustion, more careful reflection will explain 
this seeming inconsistency of thought. Whereas a state of dilatation, 
passivity or inactivity can be comprehended as of unlimited duration, an active 
constricted state, be it due to neuromuscular incitement (arterioles), or even 
to an inherent contractile power of the cells themselves (capillaries) may 
have its limitations in time, and yield to exhaustion. 

3. Specific Toxins. —This last is purely theoretical and can hardly obtain 
except in pregangrenous stages, for rubor is produced by diseases of diverse 
pathogenesis. Whilst the hypothesis of the existence of such a poison in 
thrombo-angiitis obliterans could be entertained for the acute stages of the 
disease, the chronic obstructive stage with healed products in the vessels 
should offer chemical substances not essentially different from those elabo¬ 
rated as waste or by-products in the tissues in the other occlusive vascular 
maladies (arteriosclerosis, bland thrombosis, healed syphilis with thrombosis, 
etc.) 1 


CHAPTER XLVII 

THROMBO -ANGIITIS OBLITERANS—CYANOSIS 

As a manifestation of impaired circulation, this phenomenon varies 
as to intensity, localization, and duration, and must be regarded as subject 
to vasomotor influences, as well as to obstructive circulatory factors. With 
this in mind, and with full cognizance of the influence of thermal and emo¬ 
tional factors, its role as a sign of thrombo-angiitis obliterans can be more 
accurately appreciated. 

1 It may be of interest to note here that certain Russian observers believe that in the 
course of intravascular thrombosis, a ferment or toxin is liberated that in itself can bring 
about alterations in vasomotor function. 



THROMBO-ANGIITIS OBLITERANS—CYANOSIS 


251 


Although subsidiary in importance to the rubor, it is frequently present 
over one or more or all of the toes, and even over the whole foot, especially 
when the latter is allowed to hang down for a considerable time. Then a cer¬ 
tain amount of purplish discoloration is wont to be admixed with the rubor 
that is so constantly present in this position. 

In the elevated position of the limb, when blanching has already taken 
place, multiple cyanotic areas are apt to remain, often more marked in the 
toes whose circulation has been most impaired. 

Cold has a decided influence in evoking and stabilizing an asphyctic state, 
the rubor giving way to it particularly over the very peripheral parts. But 
even under ordinary climatic conditions cyanosis of the toes is frequently 
intermingled with the rubor. Thus, the tips of the toes may be cyanotic 
whilst the dorsum shows marked hyperemia, and the plantar aspect of the 
foot may evidence patches of bluish purple discoloration. 

When considerable circulatory obstruction is present, cyanosis in the 
dependent position may yield to ischemia in the horizontal or above the hori¬ 
zontal, but patches of more or less permanent cyanosis tend to remain. 

In many cases cyanosis of the big toe is rather suggestive of the presence 
of the disease, and may be the only objective sign except for the absence of 
pulsations. That the diagnosis of thrombo-angiitis obliterans is warranted 
on these manifestations alone, the future course has demonstrated as well as 
the coincidental occurrence of the affection in the other leg where symptoms 
✓ may be pronounced. 




Local chronic cyanosis when it is limited to one toe may precede gangrene of 
that particular locality by months or even years. When it continues for a 
considerable length of time, we must be guided in making our prognostication 
as to the advent of gangrene by other signs, such as marked ischemia, a poor 
angle of circulatory sufficiency, and extensive obliteration of vessels. The 
persistence of localized and intense cyanosis, however, is always suggestive. 

In such a case observed carefully for a year, the persistence of a more 
pronounced cyanotic discoloration of the big toe of the right foot was noted, 
the cyanotic color being much deeper in the big toe than elsewhere in the 
foot. This sign was more or less constant for some ten months, when the 
rubor was intense over the whole foot except for the deep asphyxia of the big 
toe. After eleven months of almost constant cyanosis gangrene appeared. 

^ Such chronic cyanosis when edema, coldness, and localized anesthesia are 
superadded is no longer merely a sign of circulatory impairment, but augurs 
that gangrene is imminent. Amputation (Gritti-Stokes) undertaken in such 
cases has demonstrated extensive vascular occlusion involving even the 
popliteal artery although one or more vessels (such as the anterior tibial) 
may remain patent. It may be impossible even after careful anatomical/ 
investigation to establish a causal basis for the chronic cyanosis. / 

In a review of the histories of one hundred cases, the author found that 
seventy-one gave manifestations of asphyxia of one or more toes of either foot 
at some time during the clinical course, although it was not a significant sign 
at all. For, it is producible by a prolonged pendency even in the presence of 
rubor and may precede and accompany the incipiency of gangrene. In 
eighteen cases both extremities simultaneously showed cyanosis, a percentage 
of bilateral involvement that might vary considerably and be much higher if 
a longer period of observation had been undertaken. 

But cyanosis as well as ischemia (and the two often coincidentally) may 
be the expression of the concomitant action of mechanical as well as vaso- 


252 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


motor causal factors. That this is true is evidenced by the observation, that 
occasionally the forepart of the foot may be markedly asphyctic, remain so 
for a considerable period of time hour or more), and be irresponsive to 
such vasodilating excitants as changing posture (elevation and consequent 
depression) and heat. At other times, removed by but short intervals of 
time, both ischemia and asphyxia in the same foot are less marked, more 
evanescent and more readily abolished by the above mentioned means. 

It is difficult to draw accurate conclusions as to the comparative impor¬ 
tance of the vis a tergo, the hydrostatic and gravity elements, and the vaso¬ 
motor influences in the determination of the intensity of local asphyxia. 
Enough observations are at hand attesting to the participation of all of these 
factors to varying extents. Perhaps most influential are the forces of gravity 
and inadequate vis a tergo , that allow of the accumulation in the veins and 
capillaries, and a certain degree of reflux of the poorly oxygenated blood. 
Thus, we could explain the intensification of the cyanosis of the feet in the 
pendent position, and the frequent disappearance of much of the asphyxia 
in the horizontal and elevated postures. Vasomotor lability and the possi¬ 
bility of venous spasm cannot be altogether excluded, however, as an occa¬ 
sional causative or coincident and participating agent. For, while lividity 
of the fingers may be noted in the hanging position of the arms where exten¬ 
sive arterial obliteration is present, considerable or even exaggerated asphyxia 
may persist on elevation, or even when the arms are in the horizontal posi¬ 
tion. The venules probably do not empty themselves, partly because 
arterial circulation is defective or almost in abeyance in these positions, and 
also because of complicating venous spasm. 1 

An interesting case with marked cyanosis may be worthy of citation. 

W. K. complains of pain in the feet at night and the inability to sleep. Walking is 
difficult because of the swelling of the left big toe and stinging pain. Two years ago he 
could not step on the sole of the right foot which was swollen. The left big toe is now espe¬ 
cially painful and made worse either by raising the foot or lowering it. 

Physical examination.—In the pendent position the tips of the toes of both feet are cya¬ 
notic, whilst the dorsal aspect of the toes shows rubor, more intense in the left than in the 
right. The left foot is larger than the right, its forepart being slightly swollen and the veins 
standing out more prominently. The sole of the right foot shows color changes, which are 
more marked over the forepart and involve four toes. The latter show numerous cyanotic 
patches, whilst the plantar aspect of the little toe is almost normal in color. When raised 
to the horizontal the right foot becomes ischemic. All the toes of the left foot and the distal 
half of the sole show marked cyanosis, but in a few minutes the purplish tint disappears, 
leaving the sole and the toes ischemic, except for patches of permanent cyanosis. The big 
toe is tender to the touch, although without signs of trophic disturbance. The dorsum, too, 
shows ischemia when the feet are in the horizontal position. Reactionary erythromelia of 
both feet can be elicited. The dorsalis pedis, posterior tibial, and popliteal arteries of 
both legs are absent. 

Summary,—Intense cyanosis of the left foot, especially of the big toe; severe pain on 
elevation of the legs, now also in the pendent position. The right leg, previously attacked, 
is now in a latent stage. 

Temperature conditions are not without influence in determining whether 
cyanosis will predominate over the chronic rubor. Thus, in the case cited 
below we quote from the notes taken on a cool and on a warm day, to demon¬ 
strate the preponderance of cyanosis in colder weather. 

Case D. B. male, on a cool day —the right foot has a violaceous red appearance, the 
toes are livid, their tint composed of a mixture of deep bluish purple and bright red. Over 
the dorsum there is a mottling of red and blue. A similar condition obtains in the left 
foot with intensified cyanosis in certain areas, especially over the big and fourth toes. 


1 See p. 300, case S. S. S. 


TH ROM BO-A NGIITIS OB LI TER A NS—C YA NOS IS 


253 


On a warm day— the toes of both feet are bright red up to their roots. This color 
deepens in the pendent position and is attended with increasing pain. 

Pathogenesis of Cyanosis. —Cyanosis is perforce divisible into the types 
produced by the following causes: 

1. Venous obstruction. 

2. Diminution of arterial vis a ter go. 

3. Vasomotor influences. 

The most alluring explanation of the mode of production of cyanosis 
when the limb hangs down—and one accepted and taught by numerous 
clinicians—is that which presupposes obliterative disease of the veins as wholly 
responsible. Although such lesions may be a factor in certain cases, numerous 
pathological and clinical observations have demonstrated beyond per- 
adventure that cyanosis of intense degree is compatible with patent veins. 
When vasomotor influences may be discounted or excluded, the true cause 
is to be found in the diminished pressure in the arterial system, which is 
powerless to propel the blood with the usual rapidity into and through the 
devious channels, stasis in the capillaries and veins being the consequence. 
The truth of this assumption is demonstrable by the simple experiment of 
reducing the requisite force for a prompt venous return. This may be done 
by mere elevation of the limb from its situation of pendency to the horizontal 
level, where the cyanosis will immediately diminish or vanish. 

In some of the early cases 1 vasomotor instability is a decisive factor in the 
production of cyanosis giving an unusual clinical picture; this is often associ¬ 
ated with syncope, the whole making a confusing complex that antedates 
the development of the pathognomonic composite of phenomena. Where 
vasomotor action accounts for cyanosis, it is assumed by many that a spasm 
of venules occurs, that is, vascular territories distal to the arterioles suffer 
spasmodic contraction. Thus, in Raynaud’s disease even superficial veins, 
large enough to be examined by the naked eye, have been actually seen to 
contract in cases of local cyanosis, the asphyxia being thereby accentuated. 
Even contraction of the arterioles alone after producing local syncope may 
have as a natural sequence a superinduced cyanosis; and this by excluding 
the cardiovascular force—the vis a tergo —so that stagnation in the veins is 
to be expected. 

When the technic will have become perfected and standardized, estimates 
of capillary pressure may give valuable information concerning the influence 
of diminished vis a tergo and the forces impeding the outflow of blood. Capil¬ 
lary stagnation produced by the former mechanism should be associated with 
low capillary pressure, and if by the latter, with high pressure. Dilatation of 
capillaries alone could, by reason of the diminished velocity of the blood, be 
followed by relative deoxygenation and cyanosis. This is the type that 
succeeds the rubor when the limb has been allowed to hang down for a time. 
In this position the vis d tergo is insufficient to adequately accelerate the flow 
upward through the venules and against the action of gravity. We would 
not expect that the cyanosis of thrombo-angiitis obliterans developing on 
rubor would be attended with an excessive capillary pressure, unless there is 
coexisting vasomotor spasm of the venules during an attack of temporary 
or fugitive vasomotor constriction. In such, spasm of the venules may occur. 

Recent work suggests that through methods of estimating capillary 
pressure, much valuable knowledge may be gleaned as to the nature of 


1 Vide Chap. LIV. 


254 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


asphyxia. 1 If increased pressure is found, spasm of the vessels may be 
assumed, and so the participation of a vasomotor factor is believed to occur. 
Perhaps the comparative roles of the neurogenic and hydrostatic forces can 
thus be differentiated, for the latter can be wilfully altered by the position of 
the limb. So, the importance of such investigations, aside from a purely 
academic interest, lies mainly therein, that hydrostatic or mechanical factors, 
when of increasing importance, forecast an unfavorable outlook, and seem¬ 
ingly incongruous vasomotor manifestations are of relatively little significance. 


CHAPTER XLVIII 

THROMBO -ANGIITIS OBLITERANS—EDEMA 

A peculiar puffiness of the toes together with an effacement of the usual 
irregularities of the dorsal aspect of the foot is often incorrectly ascribed to 
edema alone. Although from the pathological standpoint a slight edema 
pervades the tissues, there is also a chronic proliferative process in the sub¬ 
cutaneous tissues of the toes that contributes to the picture. This more or 
less permanent condition, which is so characteristic in the cases with intense 
chronic erythromelia, may continue for years. The toes and the forepart 
of the foot by reason of the disappearance of surface irregularities, acquire 
an artificial appearance as if molded in wax. 

A transitory inflammatory edema if slight, accompanying, and due to 
the coexistence of trophic lesions such as ulcers and small patches of gangrene, 
is not at all an unusual feature nor one that need give concern. But another 
type of edema which is extensive and permanent is of great omen. 

In a number of cases, most of which curiously enough belong to the severe 
type of the disease in which the prognosis as to the integrity of the limb is 
concerned, edema is a prominent feature. Days or weeks after the onset 
of the trophic disturbances, the dorsum of the foot first begins to show signs 
of extensive edema. This is unassociated with any phlegmonous process. 
In a number of these cases the author was able to follow the course of this 
phenomenon, and found that it often accompanied or preceded sudden 
aggravation of the condition in cases in which amputation became necessary. 
In one of these cases it was necessary to amputate within two weeks after 
the onset of edema. Doubtless the edema itself, has a pernicious effect, 
acting so as to further impede the circulation of the peripheral parts (in a 
sort of vicious circle). It is apt to extend rapidly over the whole of the 
foot, and even up to the ankle and leg. 

There seems to be no doubt but that it has a bad influence upon the nutri¬ 
tion of the limb. By compressing the small vessels the compensatory hypere¬ 
mia is interfered with to a certain extent, and loses much of its efficiency in 
the nourishment of the parts. A further untoward effect is its inclination to 
increase the pain, which in these cases is already considerable in the neighbor¬ 
hood of the trophic disturbances. 

Pathological examination of the limbs in which marked edema is present 
shows the absence of involvement of the veins in so many of the cases that 
these could certainly not be held responsible, although it is possible that 
1 See Briscoe, Loc. cit. Chap. VII. 



THROMBO-ANGIITIS OBLITERANS—INTERMITTENT CLAUDICATION 255 


veins proximal to the point of amputation were occluded. Indeed, a satis¬ 
factory explanation for its production is difficult to find. It may be regarded 
as being of inflammatory origin, as the result of a lymphatic inflammation, 
although a suppurative process is certainly at hand in most of the cases in 
which it is present. 

Persistent Edema the Harbinger of Gangrene— As already stated, in 
thrombo-angiitis obliterans continued edema is exceedingly inauspicious. 
When a manifestation of inevitable gangrene, it may usher in a state of 
chronic cyanosis of the forepart of the foot, attended with marked coldness 
and anesthesia, these constituting a group of phenomena characteristic of 
one form of slowly developing gangrene. It is thus called, since weeks may 
elapse before the unmistakable and classical external signs of tissue death 
manifest themselves. The following case will illustrate. 

M. K., male, Russian, aged 35 (January 6, 1917), had had an ulcer of one of the toes of 
the right foot one year previously, and this healed slowly. For six months there were the 
usual symptoms of intermittent claudication. Following the removal of a callous (?), 
edema began to develop. This was soon attended with cyanosis; these signs with marked 
frigidity and anesthesia of the forepart of the foot were the striking and enduring manifesta¬ 
tions until amputation was done. None of the usual objective evidences of gangrene 
appeared during a period of observation from January 6 to January 18. Nevertheless, the 
pain and the persistent symptoms above mentioned attested to the assumption that the 
peripheral parts had become gravely compromised. Amputation January 19—Gritti- 
Stokes operation. 

The specimen demonstrated an absence of purulent infiltration or marked necrosis, but 
an intense ischemia of all the tissues, presaging inevitable tissue death. The popliteal and 
posterior tibial arteries were completely closed. 


CHAPTER XLIX 

THROMBO -ANGIITIS OBLITERANS—INTERMITTENT 
CLAUDICATION 

Next to the palpable signs of arterial obliteration, namely, the absence of 
pulses, this is perhaps one of the most constant features of the disease. In 
a series of one hundred cases the author obtained a history of its occur¬ 
rence seventy-eight times in one, forty-eight times in both lower extremities. 
A story of cramp-like sensations in the calf or in the foot induced by walking, 
and disappearing when at rest, may precede by weeks, months or years the 
advent of other phenomena. When associated with vasomotor symptoms, 
such as coldness, blanching of the foot, with patches of rubor alternating 
with ischemic areas, or cyanosis, the typical syndrome of Erb is present. 
However, as elsewhere pointed out, the descriptive appelation intermittent 
claudication is incorrectly applied to this composite complex of sensory plus 
vasomotor manifestations. The latter often occur in thrombo-angiitis obli¬ 
terans and other obliterative vascular diseases, unassociated with the typical 
pains and cramps induced by exertion. We prefer, therefore, to restrict the 
designation of intermittent claudication to the sensory or sensory-motor 
signs, acknowledging a certain amount of clinical interdependence of the 
two varieties. Whilst it is true that exercise may simultaneously evoke 



256 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the characteristic pains and vasomotor changes, other excitants such as cold 
and emotion may bring forth the vasomotor indications alone, unattended by 
the typical cramps. e . 

In some of the cases there is not only a history of intermittent claudica¬ 
tion, but vasomotor and sensory symptoms accompanying. The patients 
describe one or both feet as becoming suddenly white half way up the. foot 
or as far as the ankle after walking one or two blocks. They experience 
also a feeling of numbness or a “dead” feeling in the affected foot. There 
may be no pain in the foot whatsoever, or there may be pain in the calf , 
or the pain may be altogether absent. Some say that when they sit down 
after this change in color, the foot turns red or blue, this being variable 
whereas the whiteness is a more constant phenomenon. Or, ischemia alone, 
or “coldness” may be induced by exertion. 

Intermittent Claudication with Pulsating Arteries— Symptoms of inter¬ 
mittent claudication may attend apparently healthy arteries, if we accept 
the pulsations in the pedal, crural and femoral arteries as a guide. But 
one of the limbs may show advanced obliterative vascular disease, which 
should be regarded as suggestive of the development of obstructive lesions. 

We encounter cases in which one limb gives the symptoms of intermittent 
claudication for months before the pulses become extinguished. The lesions 
are probably of limited extent, and involve only the plantar or peroneal 
arteries that are inaccessible to touch. 1 

Vasomotor Symptoms with Intermittent Claudication. —The prevalence 
of vasomotor manifestations, notably coldness of the foot after walking with 
numbness and pain in the calf of the leg, in some cases of thrombo-angiitis 
obliterans has been responsible for much prejudication in the clinician’s con¬ 
ception of intermittent claudication. Whilst coldness and pallor of the foot 
may be accounted for on the basis of obstructive hydrostatic factors alone, 
wherever intensive degrees of circulatory impediment are present, there are 
equally marked examples of local ischemia and frigidity due to complicating 
vasomotor influences. Both exertion and external temperature conditions 
are influential in the production of pallor and coldness. 

It would be erroneous to regard the so-called “intermittent claudication” 
—pain in the legs and feet on walking with coldness and pallor of the peri¬ 
pheral parts—as a morbid entity. For, it has been well attested and demon¬ 
strated by the fact that most exquisite illustrations of such grouping of 
clinical features are afforded by the disease thrombo-angiitis obliterans. 
The term intermittent claudication, therefore, should be rejected as descrip¬ 
tive of a disease and restricted to a combination of associated symptoms 
observable in a number of different pathological processes. To amplify 
and explain by actual case, the following history may be worthy of study. 

Thrombo-angiitis Obliterans with Symptoms of the Sensory and Vasomotor 
Type of Intermittent Claudication. 

A. G., male, Russian, age 33 years, examined November 27, 1908, has been in this 
country twenty-one years. Smokes six to seven cigarettes a day. He has not been at work 
for about one year because of trouble with his legs that prevented walking. Illness began 
three years ago with pain in the sole of the left foot on walking. For two years the pain in 
the calf of the leg was associated with the other symptoms. He would put his foot into cold 
water and the pain in the foot would disappear. For two years he did not think it suffi¬ 
ciently severe to consult a physician, until one year ago a physician told him that he 
had rheumatism, for which he tried baths. The pain became worse, so that in October, 1907, 

1 We must not forget that seemingly authentic cases of neurogenic or angioneurotic 
intermittent claudication have been reported (Westphal, Schlesinger, Oppenheim, Chap. 
XXVI). 


THROMBO-ANGIITIS OBLITERANS—INTERMITTENT CLAUDICATION 257 


it was so severe that he could not walk at all. He would rub his toes, would suffer for hours 
with severe pain in the fourth toe and just below the fourth and fifth toes. At that time 
October, 1907, there was a little “sore” on the fourth toe. The pain was always worse at 
night. His “sore” healed after several weeks. After that he noticed that the foot would 
get pale and cold, and later would turn blue and red in the dependent position. Then last 
January he went to another physician who gave him fourteen mercury inunctions, without 
result. Then 35 injections of bichloride of mercury and potassium iodide were given with¬ 
out improvement. In fact he got worse. On walking , he says that the instep feels dead, but 
he has had no pain since the time he had his ulcers last summer. On walking, his left foot 
feels peculiar: the ball of his foot falls asleep and he is not able to walk more than six or 
seven blocks without stopping. After resting, “circulation returns” he thinks. No more 
sores have developed. Now his foot turns pale when he goes out and when he takes his shoe 
of he finds his foot white. Then , if exposed, the color returns. He feels better in warm 
weather. 

Chief complaint: Coldness of the left foot, and inability to walk because the foot 
becomes numb. 

Physical examination: The right dorsalis pedis does not pulsate; the posterior tibial 
and popliteal are present. The left dorsalis pedis is absent; the posterior tibial and popli¬ 
teal are good. 

December 1, 1908: Thrombosis of veins of both legs, involving the territory of the 
internal saphenous, is present. The patient states that his left leg gives him more trouble 
than the right. 

Physical examination: The right dorsalis pedis is absent; the posterior tibial and popli¬ 
teal pulses are present. The left dorsalis pedis and posterior tibial are absent; the popliteal 
is present. 

The left foot shows moderate erythromelia in the dependent position. The angle of 
circulatory sufficiency is about no°. 

Resume: A case of temporary recovery, the left side being more involved than the right, 
with both popliteals pulsating, and with a history of thromboses of the superficial veins on 
both sides, probably involving tributaries of the internal saphenous veins. 

February 27, 1909, physical examination: Both feet are cold to the touch. He says 
that his feet are always numb; he cannot work. No changes in the pulse on the right side 
are perceptible. The left dorsal pedis and posterior tibial are absent; the popliteal pulse 
is doubtful or faint. 

April 27, 1909: Patient says his left foot gets white at the instep as soon as he walks a 
few blocks and the foot feels dead. Has no pain. When he sits down it turns blue. The 
right foot is somewhat better, but also troubles him in the same way. He also has pain in 
the back of the left knee. Upon examination the left foot is cold to the touch, the right 
only slightly cold. 

On allowing the feet to hang down for 5 minutes the left becomes dusky, the right 
slightly blue, but there is no intense cyanosis. A peculiar brown pigmentation of the skin 
of the extremities masks the real color. At times the left foot shows a slight degree of 
erythromelia. No evidence of trophic disorder. 

Summary: Obliteration of dorsalis pedis of both legs; with posterior tibial on the left, 
with numbness and coldness as chief symptoms. No trophic disturbances. 

October 21, 1909, complains of coldness of feet and he says they get stiff. 

Physical examination: Both feet are cold to the touch, the left more than the right. 

December 8, 1909: He complains mostly of coldness of both feet and both feet become 
“ dead ” when he walks. The right foot troubles him now. He has had no sores. 

Physical examination: In dependent position, the left foot takes a dusky reddish purple 
hue, the right also shows some slight cyanosis, with a tinge of red, the color extending a short 
distance up the dorsum of the foot. Both feet are cold. The big toe of the left foot is 
cyanotic. There seems to be more cyanosis of both feet than at last examination. 
Cyanosis is more prominent than the redness; probably getting worse. 

January 3, 1910: Color of both feet pretty normal. Remarkable change in appearance, 
probably due to weather. Left, slight erythromelia. Right, still less. 

January 15, 1910: Left foot fair amount of erythromelia, and he complains of coldness 
of foot. 

February 20, 1910: Has “no feeling” in the feet. On examination left foot somewhat 
more dusky than right, but no erythromelia of either. Right big toe somewhat red. 

April 3, 1910: He is getting worse. Left foot often gets red. Now it is cold and toes 
have a reddish and bluish hue. As left is watched changes of color take place. After a few 
minutes the redness spreads over the dorsum; it is admixed with blue but is not marked. 
The right does not change color. 

October 8, 1911: Still numb legs, “without any feeling.” Color of both feet good, left 
foot much colder than the right. Coldness beginning at the toes and goes up to the ankle 
17 


258 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


on the left side, only to base of toes on the right side. Dependent position: Right almost 
normal color, left gets slightly cyanotic and red. Vessels: Right, as at last examination; 
left, also the popliteal and femoral pulses poor. 

November io, 1911: Does not feel well, feet get cold. 

On examination the left foot is slightly cyanotic, and the skin of the toes looks thin. 
In the dependent position there is no true erythromelia; but slight increase of cyanosis is 
noticeable on the left and very slight erythromelia. 

Summary: Stationary and practically cured case with both dorsalis pedes closed, but 
one posterior tibial open; and all the vessels higher up seem open. The chief signs are 
numbness and coldness of the feet, slight cyanosis and very slight erythromelia of the left. 
A case of thrombo-angiitis obliterans with varied vasomotor phenomena, and intermittent 
claudication. 


CHAPTER L 

THROMBO-ANGIITIS OBLITERANS—PAIN 

Thrombo-angiitis Obliterans without Pain. —Although pain is an almost 

certain concomitant of the other characteristic manifestations of the disease, 
it may be absent for a long period, or extensive obliteration of arteries may 
be wholly divorced of it. And so the author has observed pulseless popliteal, 
posterior tibial and dorsalis pedis arteries, with ischemia on elevation, 
reactionary or chronic rubor, without any complaint or even a recollection 
of the occurrence of pain on the part of the patient. Such are the latent or 
insidious cases described elsewhere. When two limbs are simultaneously 
, affected, one may be free of pain, the other the seat of excruciating suffering. 

Varieties of Pain. —The symptom of pain in thrombo-angiitis obliterans 
has both diagnostic and prognostic significance. It is present in a variety 
of different situations, and is occasioned by a number of diverse underlying 
causes. 

The degree of the pain is variable, not only in the stage where it is brought 
on by walking, but also when initiated by the trophic disorders and gangrene. 
In some there are distinct remissions with periods of comparative freedom, in 
others the pain is constant. When it is severe, the patient may sit with his 
leg bent at the knee holding the foot in his hand in an effort to obtain relief. 

Pain may be so mild as to be a negligible component of the syndrome. 
Or, it may be so distressing that the usual deterrent forces residing in the ego 
and preventing us from stepping outside of the bounds of propriety are nulli¬ 
fied or put into abeyance. When this occurs the patient falls a victim to 
psychoses, or his mentality becomes almost completely unbalanced, (see 
Mental Symptoms). The pain is clinically diversified as follows. 

1. Pain of intermittent claudication. 

2. Pain of acute thrombo-angiitis obliterans. 

(a) In the superficial veins (migratory phlebitis). 

0 b ) In the deep vessels (acute stage of thrombo-angiitis). 

3. Pain with changing position. 

4. Pain of ischemia. 

5. Pain with chronic cyanosis and erythromelia. 

6. Continuous pain antedating gangrene or trophic lesions. 

7. Pain with trophic disorders (fissures, ulcers, etc.). 

8. Pain with infection. 

9. Pain with gangrene. 



THROMBO-ANGIITIS OBLITERANS—PAIN 


259 


The pain may vary in situation, character, intensity, and relation to 
movement and posture. Perhaps the most common is that already described 
under Intermittent Claudication as a cramp-like and lancinating pain, or as an 
ache in the calf, ankle, or throughout the leg. Besides this, however, there 
are: (i) The vague deep seated pain attending the acute involvement of the 
deeper vessels; (2) the local and diffuse pain of complicating migrating 
phlebitis; (3) the pain associated with trophic disorders or gangrene. 

We have already referred elsewhere to that vague ache or pain which we 
may attribute to the acute involvement of the deep seated vessels. To 
what extent the pain originates in the vessel walls and how much the implica¬ 
tion of contiguous nerve is responsible, is difficult to determine. Peculiar 
“drawing” and aching sensations are described in the calf as occurring 
independent of locomotion, and may be the premonitory signs of serious, 
thrombotic invasion of the arteries. Sometimes these are of paroxysmal 
nature, lasting for several hours (1-4), of spontaneous advent, independent 
of motion and associated with tenderness to deep pressure. Such sensory 
phenomena are attributable to migrating thrombotic lesions in the deep 
vessels; they are not of ischemic or angiospastic nature. 

Although the origin of the local pain of acute migrating phlebitis is 
usually easy to recognize, the lesion may be so extensive 1 that the resultant 
pain becom'es correspondingly diffuse, ache-like and in part indistinguishable 
from that which emanates from the deeper vessels. 

But it is especially when any defect in the skin or infection occurs, that 
a severe pain in the affected region (though not altogether confined to this) 
may arise, persist and increase in intensity in a manner quite disproportionate 
to the size of the lesion. A tiny fissure—one that usually is slow in healing—- 
•often suffices to give the patient sleepless nights. Small, insignificant ulcers 
are frequently so excruciatingly sensitive and painful that until this observa¬ 
tion is oft repeated in our clinical work, we are at a loss to reconcile the objec¬ 
tive and subjective manifestations. Indeed, occasionally a patient will 
request amputation of a limb even though the indolent non-healing ulcer 
has in no sense objectively compromised the integrity of the part. And 
furthermore, even after amputation of the leg there are many instances in 
which the pain may persist for days, or even two to three weeks, or more. 
The development of this condition of intense hyperesthesia may be coincident 
with functional derangements in the centripetal sensory paths, possibly in 
the cord itself, that persist even after the original afferent impulses have 
ceased. Strange to say, however, the infiltration of the posterior tibial 
nerve behind the malleolus may cause the pain to disappear in some cases; 
but this is not true for all. It is also noteworthy that vasomotor phenomena 
not uncommonly appear with or after the advent of the pain, seemingly in 
some reciprocal relationship. As to whether the continuous sensory impulses 
are at all responsible for the creation of vasolability through 'higher centers 
is a matter worthy of further study. 

The pain of intermittent claudication is described in detail under the 
chapter on Intermittent Claudication. Attention is called here merely to 
the method of differentiating this symptom from similar and coincident pain 
due to other causes. When a patient who has discomfort, cramps or pain 
“throughout the leg” or in the calf or ankle, or on walking, but also has had 
acute attacks of pain independent of locomotion, the latter may under 
certain circumstances be referable to recent active thrombosis in some of the 
deep vascular territories of the leg. 

1 See fulminating cases, Chap. LVIII on Migrating Phlebitis. 


260 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The pendent position frequently intensifies the pain in the leg and foot, 
and is described in some instances as coming on as soon as the patient gets 
out of bed. 

Because of conflicting statements, it is often difficult to draw definite 
conclusions as to the influence of position. The history may reveal in the 
case of one limb that the pain is increased in the pendent position and 
aggravated by elevation in the case of the other. 

Sequence of Various Types of Pain. —Most commonly a period of inter¬ 
mittent claudication antedates the intense, more delimited pain. Such a 
stage is often treated as “rheumatism” without relief to the patient. Then 
follows a period of constantly increasing pain in one or more toes, which may 
be designated as a tropho-prodromal 1 sign, since it usually forecasts the advent 
of fissures, bullae or other trophic lesions and even gangrene. With the 
onset of such lesions a marked increase in the intensity of the suffering can be 
expected, the latter diminishing and even disappearing with the healing of 
open wounds. Just prior to or after the cicatrization of such lesions there 
may be a stage of vasomotor derangement. At this time coldness, pallor and 
numbness, with their attendant discomforts, may modify the sensations 
described as “pain” by the patient. 

Continuous Pain in Toes. —When the patient begins to complain of 
continuous distress and then of pain in one or more toes, the disease is usually 
well developed, and the trophic type of lesions or even gangrene is to be 
expected. Change in color of the affected toes to a distinct or angry red in 
the pendent or horizontal position is then also! noted by the patient, except 
in those more uncommon cases where the vasomotor blanching seems to 
dominate in the clinical picture. A good illustration of the advent of the 
constant type of pain is offered by the following case. 

S. W., male, aged 37, began having pain in calf of left leg when walking but short distance 
2^2 years ago. A year and a half ago continuous pain in the left big toe set in, which subse¬ 
quently spread to the second, third and fourth toes. In spite of a 4 week stay at a hospital, 
the symptoms did not subside. 

Seven weeks ago the same pain previously described in the left leg appeared in the right 
leg, associated with discoloration of the toes and severe pain in the fifth toe. A fissure 
appeared on the fifth toe because of which the nail was removed. 

Four weeks ago the tip of the left big toe became very painful, a bleb appeared which 
subsequently apparently healed, leaving the region of the nail very painful. 

Physical examination: In the horizontal position the forepart of the left leg shows 
moderate erythromelia, and there is moderate hyperemia over the greater part of the 
dorsum. The big toe is swollen particularly over the outer part of its distal phalanx, and 
there is an accumulation of serum under the nail. 

In the horizontal position the right foot shows slight erythromelia. The fifth toe is 
slightly swollen, and presents a fissure on its plantar aspect where the nail was removed. 

In the dependent position both feet soon become angry red. In the elevated position 
the color leaves the big toe of the left foot first, this toe becoming completely blanched 
within a few seconds. Cyanotic patches are apparent over the second and third left toes, 
and rapid blanching of the entire foot, with the exception of the cyanotic patches previously 
described, takes place. The right foot, too, shows marked blanching in this position. The 
patient complains of severe pain when the legs are elevated. 

The external iliac and femoral arteries of both lower extremities pulsate; the right popli¬ 
teal is present, the left absent as also both posterior tibials and dorsalis pedes. 

Tenderness. —This would seem to be an almost inexplicable phenomenon 
in many cases and at certain stages of the disease. In its most exquisite 
form it accompanies trophic disorders of rather limited extent, when these 
manifest themselves as ulcers or deep fissures near the tip of the toe, especially 
near or at the nail bed. 

1 The word is coined to denote that which is a harbinger of trophic disturbances. 


TH ROM BO-A NGIITIS OB LI TER A NS—COLDNESS 


261 


Its existence bespeaks the presence of one of the following conditions: 
(i) migrating phlebitis; (2) the acute involvement of the deep vessels (deep 
tenderness); (3) chronic cyanosis, or more or less chronic ischemia of the toe 
whose nourishment is most impaired (impending or imminent gangrene); 
(4) trophic lesions (fissures and ulcers); and (5) gangrene. 


CHAPTER LI 

THROMBO-ANGIITIS OBLITERANS—COLDNESS 1 , 

Coldness of one or more toes or fingers is a common complaint, and, 
according to the anamneses and records of physical examination, its advent 
is influenced by a number of different factors. These are exposure to cold or 
inclement weather, washing in cold water, walking, and more rarely, emotional 
strain (vasomotor) frequently described by the patient as “excitement.” 

Just as in the case of the ischemia, rubor and cyanosis, so also here sub¬ 
jective and even objective diminution of temperature is produced either by 
(A) neurotic (vasomotor) causes, or (B) by abnormal mechanical or hydro¬ 
static agencies. 

A. Neurotic Types. (1) Transitory Vasomotor Coldness. —After a pro¬ 
dromal stage of intermittent claudication, “coldness and numbness” of one 
or both feet may be the striking features in the clinical picture. When pro¬ 
voked by walking there ensues the syndrome dignified into a morbid entity 
by Erb. If the sensory and vasomotor symptoms—that is, the cramps, pains, 
the pallor and coldness of the parts be alone taken into consideration, “inter¬ 
mittent claudication” will be diagnosticated, whilst, in truth, we will have at 
hand manifestations of a pathological and clinical unity—thrombo-angiitis 
obliterans. 2 

(2) Prolonged Vasomotor and Hydrostatic Coldness {with Ischemia). —When 
coldness with or without ischemia in the horizontal position is protracted, 
we are dealing with a stage in which vasomotor influences exert a pro¬ 
longed effect on the superficial capillaries and arterioles—an influence 
quite out of proportion in intensity to the degree of organic circulatory inter¬ 
ference. Thus, when a patient complains that the toes and foot have been cold 
(and possibly white) for some time, although not through twenty-four hours of 
the day, and the sensation is regularly evoked by the horizontal posture as 
also by exposure to cold, we must differentiate between coldness and pallor 
due to hydrostatic influences alone—lack of adequate distribution of blood— 
and that partially motivated by vasomotor activities. Because clinical and 
pathological observations have shown that coldness and pallor in the hori¬ 
zontal do not go hand in hand, in a given case, with the extent of intra¬ 
vascular obstruction, but that both manifestations may disappear as more 
and more arterial territory becomes obturated, the rdle and significance of 
complicating and associated neurotic agencies becomes clear and comprehensible. 

1 Because of the intimate association of coldness and ischemia, the description of these 
two manifestations must needs overlap, so that the two chapters are best studied together. 

2 For an excellent illustration of the symptoms here mentioned refer to Chap. XLIX, 
Intermittent Claudication; also see Chap. XXVI. 



262 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


We assume that by virtue of an excessive lability of the vasomotor mech¬ 
anism in some cases, the partial circulatory depletion (partial ischemia) 
occasioned by elevation of the limb to the horizontal is sufficient to elicit 
disproportionate vasoconstricting response, extending to and implicating 
particularly the superficial capillaries and arterioles. We have contended 
and attempted to explain elsewhere 1 that a neurotic reaction is induced by 
raising the leg ninety degrees above the horizontal. 

So, by a combination of two wholly diverse mechanisms, subjective and 
objective phenomena described as “coldness and whiteness or pallor” are 
brought into being. 

When coldness and pallor occupy but a relatively short period of the 
clinical history and vanish either completely or in part with progressive 
aggravation of the pathologic lesions, we are justified in assuming other than 
merely obstructive agencies as responsible. 

It is well, therefore, to attempt to differentiate in making a physical 
examination between the role of mere elevation of the extremity, or insuffi¬ 
cient blood supply from the vasomotor influences. Such power of appraise¬ 
ment can be gained by experience. 

Another set of hypotheses may be applicable here, too, as previously 
offered in explanation of other vasomotor phenomena; namely, the local 
influence of metabolites, 2 (or possibly specific vessel toxins), and the inherent 
independent functional activity of the capillaries and venules themselves. 3 If 
such additional factors be accepted, it is clear that the regulation of the periph¬ 
eral circulation in the extremities (as also in organs) is necessarily 
exceedingly complicated and not always divisible into its several causal 
influences. 

B. Coldness Directly Attributable to Vascular Occlusion. —This, too, may 
be subjectively or ob jectively demonstrable. The variations in normal suscep¬ 
tibility to the feeling of “ cold” of the extremities, in individuals whose cardiac 
and vascular systems are apparently normal, is a matter of common— 
knowledge. So here, too, the neurogenic and emotional factors cannot be 
excluded and their presence may obscure an otherwise clear reciprocity 
between arterial disease and thermic conditions. A certain restraint, there¬ 
fore, must be exercised in the interpretation of “coldness” both of subjective 
and objective varieties. Some patients with but limited invasion of arterial 
territories describe “coldness” as an annoying and persisting complaint; 
whilst others rarely notice it—except under special climatic conditions 
—even though the arteries are extensively compromised. Where a limited 
part of the foot, such as one or more toes, are continuously cold, often pain¬ 
fully so, over a protracted period, and objective signs correspond, the pheno¬ 
menon is of grave import and often initiates a trophic disorder or gangrenous 
lesion. 

Although a certain degree of coldness is common to most of the cases, there 
is a kind of frigidity that accompanies the severe types of gangrene. In some 
of these cases where sudden and extensive gangrene may take place, not only 
the foot, but also a quarter, a third, or a half of the leg will be intensely 
cold, so that we almost fear that an occlusive thrombosis has occurred. 

Objectively we should examine all cases of suspected organic obstructive 
vascular disease of the extremities by a comparative method of palpation, 
both as to differences in the warmth of the corresponding extremity, and in 

1 Chaps. XLV and LIV. 

2 Chap. VII. 

3 See Chaps. CVII and CVIII; also group 5, p. 578. 


THROMBO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 263 


the temperature at different levels. It is a good procedure to pass the palm 
of the examining hand slowly from the knee (first in front, then behind) 
towards the foot, noting the degree of warmth or cold, and the upper limit 
of the zone of frigidity, if such be present. Then each toe should be 
separately tested and compared with the others of the same foot as well as 
with those of the other foot. 

Perhaps one of the most valuable objective methods of roughly appraising 
the quantitative influx of blood into the lower extremities, is a search for this 
level of distinct lowering of temperature. To this end, we first eliminate those 
factors that may lead to fallacious interpretation, to wit: the effects of imme¬ 
diately prior exposure to cold and vasomotor instability. Then, by passing 
the warm palm of the observer’s hand in close contact with the extremity from 
above downward, and by a comparison with the other side, changes as well as 
definite coldness at certain levels will be appreciated. Similar methods are 
applicable to the upper extremity. 

As a test for the response of the circulation to special circumstances, such 
as exercise, thermic influences, etc., the search for the degree and level of 
coldness is also of some value. Single observations, however, must be dis¬ 
carded as insufficient and unreliable; repeated ones may throw some light on 
the prognosis. 


CHAPTER LII 

THROMBO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 

A. Absent Pulses. —As an indication of organic arterial disease, a lack of 
beat in the dorsalis pedis, posterior tibial, popliteal, and femoral arteries is a 
most reliable sign. In thrombo-angiitis obliterans, a malady that usually 
comes to our notice after advanced inroads on the integrity of the arterial 
and even venous distribution of the extremities have occurred, an absence of 
at least the dorsalis pedis and posterior tibial pulses is to be expected. The 
occlusion begins for the most part in the peripheral arteries, in the plantars, 
dorsalis pedis and their larger branches, and it is not long ere the expansile 
activities of these vessels cease. However, the variations in the intensity 
and site of the pathological alterations are sufficiently great to make us cogni¬ 
zant of the incidence of a stage or clinical period in which no tangible evidence 
of arterial obliteration is at hand. 

Arterial Pulsation in Certain Early Cases .—Although we must concede 
the diagnostic value of lack of pulsation in thrombo-angiitis obliterans, 
normal arterial beats are demonstrable even in the peripheral vessels (that is, 
dorsalis pedis and posterior tibial) in some of the “early” cases. It is not 
only theoretically possible, but has been proven beyond peradventure by 
clinical and pathological observations, that a number of the other char¬ 
acteristic objective phenomena of thrombo-angiitis obliterans may ante¬ 
date by weeks or months the disappearance of either the dorsalis pedis or 
posterior tibial pulses. Thus the following sequence of events in a certain 
case will illustrate. 

(i) At the first examination the vessels are found pulsating; ischemia and 
erythromelia absent. • 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


:€4 


(2) A period of pain in the calf of the leg with tenderness and some cyanosis 
in the pendent position, the vessels still pulsating. 

(3) The development of marked ischemia on elevation, pain persisting, and 
still no change in the pulses. 

(4) Finally, the disappearance of the pulses. 

Again, in other early cases, with the accessible arteries beating, the 
absence of corresponding pulsations in the other leg, with other symptoms, 
should arouse our diagnostic suspicions. Or, the existence of a solitary sign, 
such as ischemia on elevation with or without a history of intermittent claudi¬ 
cation or migrating phlebitis, is incontrovertible evidence of the advent of 
further trouble and of the coincident involvement of arteries beyond the pale 
of examination by palpation. If we follow carefully the clinical course of such 
early cases, we will note a progressive disappearance of the pulses, usually in 
the following sequence—the dorsalis pedis, then the posterior tibial, and then 
the popliteal. In what period of time this may occur is illustrated by the 
following case. 

H. R., age 32, Russian Hebrew, first examined by the author on August 17, 1908, had 
had pain in the toes of the left foot 5 years previously; then cramps in the legs up to the 
knees on walking, over most of the subsequent period. A few weeks before examination he 
was treated for “phlebitis’’ of the right leg, that had existed for almost 5 months. 

August 17,. 1908, right leg: All the vessels pulsate but vasomotor phenomena are present 
as also ischemia on elevation. The left leg shows absence of pulses in the dorsalis pedis and 
posterior tibial, marked erythromelia, ischemia on elevation—a typical example of thrombo¬ 
angiitis obliterans. 

December 1, 1908, persisting vasomotor phenomena in the right leg— vessels still pulsate. 

February and March, 1908, the dorsalis pedis and posterior tibial arteries of the right foot 
no longer pulsate. Left foot—beginning trophic disorder of the big toe; gangrene to be 
expected. 

March 1, 1909, amputation of the left leg. 

June, 1909, marked disturbances in the right foot on allowing weight to rest on it, and 
burning pain in the foot when he walks a short distance with the aid of crutches (thus the 
typical thrombo-angiitis obliterans symptoms are now well developed in the right leg 
appearing pari passu with the extension of the obliterative process as estimated by investi¬ 
gation of the pulses). 

In this instance the disappearance of the dorsalis pedis and posterior tibial 
pulses within a period of 7 months was coincidental with the transformation of 
a case of exquisite vasomotor symptoms , into one with the usual attributes of 
true thrombo-angiitis obliterans. Other signs, however, synchronous with 
the neurotic manifestations, made the diagnosis of organic arterial occlusion 
acceptable, even at the first examination. 

Pulsation Absent in All Arteries of a Limb. —While it is tempting to 
prognosticate a severe clinical course when arterial occlusion over vast 
extent is objectively demonstrable, experience teaches that symptoms may 
be absent or slight , with obturation of all the accessible vessels of the lower extremi¬ 
ties 1 including the external iliac artery. 2 So we note a group which may 
be described under the above caption. Here belong: 

(a) Cases without symptoms. 

(b) Cases with minimal or insignificant symptoms. 

(c) Cases with one or both limbs compromised early and lost. 

(a) Cases without symptoms, demonstrate the insidious onset and develop- 


1 For brevity the words “of the extremity” being implied and self-understood, are 
frequently omitted in the text. 

2 It may be recalled here that absent or imperceptible pulsations are not, accurately 
speaking, identical with obturated vessels (Chap. XXIV). 


TH ROM BO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 265 

ment of the disease and the apparent unimportance of multiple pulseless 
vessels. Such cases, however, are rare and are candidates, as it were, for 
immediate conversion of a dormant into an intensely active and severe 
clinical course upon the least insult. An instance of this type has been 
recounted in Chap. XLII, p. 220. 

(ft) Cases with Insignificant Symptoms. —The absence of many pulses 
does not imply that we are more apt to find trophic derangements. Indeed, 
where there is a paucity of manifestations extensive arterial obliteration is one 
of the striking features in thrombo-angiitis obliterans, as well as in arterio¬ 
sclerosis. Many of the “latent cases” and those examples where only one of 
two affected lower extremities is complained of, evidence lack of pulsation in 
both arteries of the foot, in the popliteal or even the femoral. Where clinical 
proofs of disease are apparent, these may be minimal, often represented 
merely by intermittent claudication, frigidity of the foot in cold weather, 
possibly with attendant attacks of migrating phlebitis; but trophic derange¬ 
ments and gangrene may be absent. The following excerpt from an illustra¬ 
tive case merits brief citation. 

Obliterated dorsalis pedis , posterior tibial, popliteal and femoral arteries 
without trophic disorders. 

A. G., 42 years of age, Austrian Hebrew, on February 12, 1909 gives a history of having 
had trouble in the right foot and leg for about 22 years, difficulty on walking and pain. 
Until 1 year ago, however, this was not sufficient to give him any concern; but for the last 
11 months the pain has been so marked over the inner side of the ankle after walking, that 
he is trying to obtain relief by means of arch supporters. In addition he has noticed nod¬ 
ules in the skin. Six weeks ago such a red nodule appeared under the skin at about the 
middle of the right leg. He can go no farther than 1 or 2 blocks at a time. 

Physical examination: The right leg is distinctly paler than the left, but there is no 
chronic erythromelia. All the vessels of the left leg pulsate. On the right side, however, 
the dorsalis pedis, posterior tibial, popliteal and femoral arteries do not pulsate; the external 
iliac beat is only faint. On elevation the right leg blanches distinctly. 

During December, 1909, and January, 1910, while under observation, he had recurrent 
attacks of migrating phlebitis involving the region of the right calf and the inner side of the 
ankle. 

A typical case, then, of thrombo-angiitis obliterans combined with migrating phlebitis, 
and without any trophic disturbances in spite of the very extensive vascular occlusion, all of 
the usual pulses being imperceptible, except a very faint beat in the external iliac artery. 

On close observation of many cases with perceptible beats in certain or 
all of the usual situations, the advent of extinction of the pulse can be 
demonstrated. 

H. R. showed an absence of the posterior tibial and dorsalis pedis pulses of the left leg 
(the limb more markedly affected), whereas the same vessels of the right leg were beating 
strongly (August, 1908). In December, 1908, the dorsalis pedis beat of the right foot could 
no longer be elicited. Later in the month the posterior tibial pulse was also absent. In 
June, 1909, the popliteal, too, became imperceptible. Therefore, within 1 year (about 
10 months) all three pulses, posterior tibial, popliteal and dorsalis pedis disappeared in the 
right limb. 

Intermittent claudication and possibly a “sore” over one toe which may 
heal, may be the only manifestations. Thus, the following is an example. 

B. B., 1 aged 34 years, Russian Hebrew, when examined June 17, 1909, gave a typical 
history of migrating phlebitis with trouble in the right leg for 8 years, and in the left leg for 
3 years. For 2 years, intermittent claudication in the left leg had been present, and in 
January of this year a small sore appeared at the tip of the left big toe. His chief complaint 
was “trouble” with the other leg, and except for some coldness and numbness of the left 
foot, this extremity gives him little concern. 

1 See Chap. LVIII, p. 286. 


266 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

Objectively the signs of thrombo-angiitis obliterans of both lower extremities are strik¬ 
ing, and the femoral, popliteal, posterior tibial and dorsalis pedis of the left leg tail to 
pulsate. 

(c) Cases with One or Both Limbs Compromised Early and Lost. It may 
be called to mind here—for it will be elsewhere described in extenso and 
illustrated by clinical example—that there is an acute fulminating thrombo- 
arteritis and phlebitis involving the deep vessels, as well as of the superficial. 1 
The invasion of a large vascular territory may take place within a brief time, 
contrary to the general rule. 

B. Pulses Present —Valuable as the positive finding of imperceptible 
pulse may be, the existence of pulsations throughout all of the usually 
palpable arteries of the lower extremities may not preclude the presence 
of thrombo-angiitis obliterans or other obliterative or occlusive vascular 
affection. Occlusion of certain vascular territories may escape our diagnostic 
means of interpretation; and we must have recourse to other concomitant, 
complicating signs and complexes for diagnostic conclusions, when the affec¬ 
tion is restricted to the confines of these. Such regions are the peroneal, 
digital, and plantar arteries. 

Of the many bizarre pictures that thrombo-angiitis obliterans affords, 
the following apropos of the above observation, may be cited. 

Thrombo-angiitis Obliterans with Pulsating Arteries. 

M. R., Russian, male, aged 40, when seen November 24,1908, stated that 6 years ago he 
had “rheumatism” of both feet, with pain becoming progressively worse in the toes and 
most marked in cold weather. The pain was finally alleviated by heat and disappeared 
until 2 years ago, when it recurred most intensely in the middle toe of the left foot. After 
the application of a carbolic solution, spontaneous gangrene of this member occurred, 
necessitating amputation. . , . 

Although gangrene of the fourth toe of the right foot presented itself 1 year ago, this 
disappeared leaving trophic disturbances of the nail. One month ago there were trophic 
disturbances of the middle toe of the right foot and small toe of the left. He further stated 
that both feet had been red since 2 years. 

Physical examination: Slight cyanosis of the left small toe, amputation of the third, 
otherwise the left foot appears normal. There is marked cyanosis of all the toes of the 
right foot, most intense in the third. 

Upon elevation, slight ischemia of both feet can be elicited. 

In the dependent position there is intense cyanosis of both legs, admixed with patches 
of red; exquisite pain in this position. 

Vessels: Both dorsalis pedes, posterior tibials, and femorals pulsate strongly, the poph- 
teals are weak. 

November, 1908, amputation of the right middle toe for gangrene. December 29,1908, 
returned to hospital because of gangrene of the left little toe. 

Physical examination: Bleb over little toe of left foot, filled with pus, erythromelia of 
rest of toe; remaining toes normal; no cyanosis in dependent position. 

January 4, 1909, disarticulation of left little toe for gangrene. 

January 15, outer half of dorsum of left foot slightly reddened. 

January 20, still erythromelia of the left foot, no cyanosis in the dependent position, 
ischemia on elevation. 

Evidently since November, 1908, ischemia on elevation has developed , a significant 
evidence of organic vascular lesion. 

March 21, 1909, on allowing feet to hang, they soon become cyanotic, the blue discolora¬ 
tion being admixed with patches of erythema; soles of both feet pinkish in color; all vessels 
pulsate. 

C. Pulsations Disappearing under Observation. —Were it possible to 
keep cases confined to bed for many months under daily observation, the 
manner of invasion of new vascular territories particularly in more or less 
approachable sites could be well studied, and valuable information acquired. 
This is particularly true as applied to that portion of the posterior tibial 

1 See p. 372, Case I. L., also p. 291, Case H. H. 


THROMBO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 267 

artery that pulsates behind the internal tibial malleolus. We shall refer 
elsewhere to what the histories have conveyed in this matter. 

Certain interesting data relative to time and advance of the disease, and 
to the significance of added vascular involvement in the symptomatology, 
could be derived from a less continuous but frequent study of cases over long 
periods of time (several years). 

The Severity of the Symptoms Corresponding to Arterial Occlusion — 
While this caption emphasizes a truism which is applicable in many cases, 
it needs qualification in two different senses. For, we have learned firstly' 
that extensive arterial occlusion may be adequately compensated for by 
collaterals and have no subjective concomitants (Chap. XLII) and 
secondly, that the presence of pulsation in certain vessels may be associated 
with widespread obturation in many distal and concealed channels. Thus, 
a patent posterior tibial is not significant if the plantar, dorsalis pedis' 
dorsalis hallucis and possibly also the peroneal arteries are closed. 

Importance of the Popliteal Pulse. —The disappearance of the popliteal 
may correspond to aggravation of symptoms. So, in a case (D. B.) the 
course may be summarized as follows: 

D. B. in 1896, had migrating phlebitis over the left thigh; 1899, phlebitis over right calf. 

In 1904, migrating phlebitis in left antecubital region involving the median cephalic vein 
and one of the anterior ulnar veins. A specimen removed for microscopic examination 
showed acute inflammatory lesions that were not correctly interpreted at that time, but 
after subsequent studies by the author, the lesions were recognized as being those of the 
acute phase of thrombo-angiitis obliterans. At the same time the patient had prodromal 
pains in the ankle of the left foot with some cyanosis in the pendent position. 

In January, 1907, the posterior tibial, and dorsalis pedis arteries of both feet did not 
beat, both popliteals did. 

February, 1907, symptoms, especially referable to the upper extremities were noted, 
some pain on walking and rubor of the left foot. 

In December, 1907, the usual symptoms of thrombo-angiitis obliterans in both legs. 

January 3, 1908, both posterior tibials pulseless, both popliteals beat strongly. 

February 7, 1908, right popliteal pulse strong; left diminished. 

. September 7 ;> 1908, right popliteal pulse has disappeared, with this, distinct aggravation 
m condition of right leg and more pain. 

November 19, 1908, pulsations the same, left popliteal still present. Up to early in 
1908 the left leg was distinctly worse, the right popliteal pulse better than the left. Since 
then there was marked intensification of symptoms on the right side with absence of the 
popliteal pulse. In both feet there are rubor and cyanosis with ischemia on elevation. 

April to June, 1909—ulcers of both feet; condition of both aggravated and all of the 
pulses except the femorals and iliacs, are now absent. 

Almost simultaneous loss of the popliteal pulse with increase in the 
severity of the symptoms, followed by gangrence and amputation is 
llustrated by the following case. 

S. S., February 5, 1910, migrating phlebitis 1908, 1 year ago intermittent claudication. 

February 6, 1910, evident involvement of both lower extremities, dorsalis pedis and 
posterior tibial arteries pulseless, all others patent. 

March 20, 1910, aggravation of condition in both legs. 

January 3, 1911, right foot looks somewhat withered, simulating sclerodactyly, a dead 
patch of skin over the big toe, right popliteal pulse now absent. 

January 28, 1911, Gritti-Stokes amputation (right). 

Disappearance of Pulses Compatible with Arrested Symptoms. —To conclude 
that progressive arterial occlusion should correspond with an exaggeration in 
the extent and degree of the complaints, would be a universally warrantable 
assumption, were it not for the occurrence of the following two types of 
clinical complexes, first the dormant obliterative process without subjective 
signs, and second, the inverse type in which “apparent healing” with cessa- 


268 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


tion of subjective phenomena or even regression of objective manifestations 
may take place. 

The cases exemplifying the loss of pulsation unattended with subjective 
and objective alterations perceptible to the patient have been described on 
p. 220, 6. They seemingly invalidate and nullify the deductions derivable 
from the presence of pulseless vessels. Our ability to elicit other coincident 
signs of which the patient is unaware fortifies the diagnostic value of the silent 
vessels. Such indications elsewhere alluded to, are notably ischemia on 
elevation, chronic or induced rubor and possibly the demonstration of a 
diminished angle of circulatory sufficiency. 

To illustrate the two opposed dicta, we may cite in brief the salient facts of 
the following history, showing: 

i st, that pulses disappear pari passu with progressive sensory and circu¬ 
latory manifestations; and 

2nd, that they are absent while symptoms regress and the latent or 
arrested stage is being developed. 

M. C., aged 24 years, with the usual prodromal symptoms, when examined March 18, 
1908, gave these physical signs; left leg in a state of erythromelia, dorsalis pedis absent, 
all other pulses present; right leg shows doubtful ischemia, all vessels beating. 

November, 1909, the left leg “cured” as far as the subjective manifestations are con¬ 
cerned, but erythromelia persists; dorsalis pedis pulse absent, posterior tibial very faint. 

The right leg now gives him trouble, intermittent claudication and a trophic ulcer over 
the big toe are present. The dorsalis pedis and the posterior tibial arteries do not beat.. 

February 12, 1910, under conservative treatment the gangrenous area on the right big 
toe has practically healed, and the dorsalis pedis and posterior tibial arteries of both legs 
are pulseless. No symptoms on the left, objectively erythromelia is present. 

Epicrisis. —Closure of two vessels of the right, one of the left leg, while under observa¬ 
tion, with aggravation of symptoms in the former, improvement in the latter. 

Such antagonistic clinical states when viewed in relation to advancing 
vascular obturation, can only signify and emphasize that the state of the 
collateral paths plays just as important a role in symptomatology as the quanti¬ 
tative circulatory impediment. 

Sequence of Loss of Pulsation. —A careful search for the inception of the 
occlusive process in the pulsating arteries discloses the following as the usual 
chronological sequence in loss of beat: first, in the dorsalis pedis, then in the 
posterior tibial and popliteal, and finally, in the femoral and external iliac 
artery (the latter being but rarely affected). No inflexible rule, however, is 
applicable, since the closure of the posterior tibial artery behind the malleolus 
may antedate loss of pulsation in the dorsalis pedis, an indication, too, of 
prior and more extensive disease in the plantar distribution. 

The advance of the lesion may occur so rapidly that within 1 year or less, 
all the pulses of one extremity may be missing, although symptoms may be 
moderate and gangrene absent. 

J. A., February 26,1907, case with intense blanching of the right foot on exposure to cold 
and on walking, began 1 year before with sudden attack of inability to walk, there being no 
definite localization of the pain, which was referred to the whole leg (an acute attack of 
thrombo-angiitis obliterans?). All of the usual vessels of the right leg are pulseless; the 
big toe is pale, the others slightly cyanotic. 

If a patient be kept long enough under observation, the dorsalis pedis or 
posterior tibial pulses, or both, may be observed to become extinguished. 
Occasionally, other symptoms such as intermittent claudication may pre¬ 
cede the loss of certain pulses. For, intermittent claudication may depend 
on the closure of deep arteries beyond the realm of diagnostic palpation. 


THROMBO-ANGIITIS OBLITERANS—ARTERIAL PULSATION 269 


Intermittent claudication may appear before the advent of erythromelia. The 
following case will illustrate:— 

F. K. }> Russian Hebrew, 24 years of age, November 5, 1907, had evidently been troubled 
mostly with the big toe of the left foot; and amputation became necessary. There was, 
however, a distinct history of pain in the right calf. On physical examination the right 
dorsalis pedis pulse was distinctly palpable, although the left was not palpable. May 27, 
1908, the beat in the dorsalis pedis of the right leg disappeared. The intermittent claudica¬ 
tion antedated the disappearance of the pulses by a considerable period. 

Relation of Pulsation and Clinical Duration. —So capricious are the 
exacerbations of this disease, that no conclusions as to the age of the process 
should be drawn from mere clinical observations alone. The extremity 
affected for many years may show fewer pulseless vessels, and be in better con¬ 
dition than the other in which symptoms have been noted but recently. 

B. B., after symptoms in the right leg for 8 years, with the left implicated for 3 years, 
demonstrated clinically a more extensive disease of the latter when none of the pulses could 
be elicited, while a good femoral beat was present in the other extremity. The other object¬ 
ive and physical phenomena, too, gave testimony to the more grave vascular impairment 
of the left in a smaller angle of circulatory sufficiency and more marked ischemia. 

Pulsation and the Angle of Cirulatory Sufficiency. —The number of pul¬ 
sating vessels is not always in harmony with adequacy of circulation, nor 
is it in consonance with the angle of circulatory sufficiency. Thus, this 
may be less than 90°—and evidence of marked impairment—and still the 
popliteal and other arteries may be pulsating. In other patients, however, 
where we find both legs involved, the palpable extent of vascular obliteration 
corresponds fairly well with the intensity of the other signs. So, erythro¬ 
melia and ischemia may be most marked on the side where all three vessels of 
the leg and foot are found pulseless. In one case (B. H.) 3 vessels were pulse¬ 
less on the left side and 2 on the right, with a corresponding development of 
the symptoms. 

D. Pulses of the Upper Extremities. —A more detailed record of the 
involvement of the radial and ulnar arteries will be found in the chapter on 
the Upper Extremities in Thrombo-angiitis Obliterans. Here we will simply 
allude to certain peculiarities in the relationship between evidences of arterial 
obturation and symptomatology. 

The radial pulse may vanish during the period of clinical observation 
without any other clinical signs referable to such closure. 1 

The radial pulse may become extinct simultaneously with the manifes¬ 
tation of an acute thrombo-arteritis and periarteritis; but there may be no 
other symptoms save those referable to the local alteration in the recently 
occluded and inflamed vessel. 

Vasomotor symptoms may antedate the disappearance of the radial pulse, 
in which case differentiation from the vasomotor neuroses may be difficult or 
almost impossible. The unilateral appearance (asymmetrical) of the affec¬ 
tion speaks in favor of thrombo-angiitis obliterans. 

A further discussion of this phase of the subject will be found in Chap. 
LIX. 

E. Return of Pulsation. —Observers report return of pulsation in arteries 
that had been seemingly obstructed; and, in personal communications from 
clinicians, this fact has been made note of. That pulsation cannot return in 
an artery, that is completely closed through the lesions of thrombo-angiitis 
obliterans, we are convinced from the pathological changes. However, 


1 Case J. A., p. 295. 


270 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


dissection of numerous amputated limbs has given a clue as to the possible 
cause of the reported reestablishment of the dorsalis pedis and anterior 
tibial pulses, and it is these vessels in which the observation has been most 
frequently made. A glance at Figs. 47 and 56c will demonstrate how 



Fig. 47.—Representation of the patency of certain vascular territories in thrombo¬ 
angiitis obliterans, and its possible effect on the perceptibility of the pulses. 

sections of the anterior tibial or dorsalis pedis artery in their palpable por¬ 
tions may remain patent, whilst the central more proximal parts may be 
partly or completely occluded. In such cases the artery is more or less 
collapsed, or allows a small amount of blood to trickle through, or the 
circulatory force therein is insufficient to produce a beat. With increasing 
and improving circulation through collateral paths, pulsation may become 
reestablished, the blood flowing through devious channels in uninvolved 
territory. 


CHAPTER LIII 

THROMBO-ANGIITIS OBLITERANS—MENTAL SYMPTOMS 

The gloomy outlook in this malady has become so well known to a certain 
class of the population in many of our 1 big cities, that the dread of the conse¬ 
quences surpasses even the fear of the necessary attendant endurances. 
Thus, amongst the more highly educated (including physicians), temporary 
neuroses are not uncommon, often aroused by fancied or simulating manifes¬ 
tations in the extremities. When one or the other of the subjective symp¬ 
toms of thrombo-angiitis obliterans persists, and when no adequate causal 
explanation is forthcoming, even in the absence of closed vessels or the char¬ 
acteristic objective signs, we should regard the case as a suspect, although 
allaying the patient’s apprehensions as much as we can. 

The patients who have run the gamut of many distressing lesions, severe 
intermittent claudication, exceedingly painful toes with or without ischemia 

1 United States. 










THROMBO-ANGIITIS OBLITERANS—VASOMOTOR SYMPTOMS 271 


or cyanosis, severe and even excruciating local pain, associated with fissures, 
ulcers and gangrene, with inability to walk, possibly with the experience of 
single or multiple amputations of parts of one or more limbs—in these it is 
not surprising that with increasing calamitous happenings and constant 
attention to their ills, the afflicted should retire into their subjective world, 
where the intolerability of their own physical status is paramount. 

A haggard look, the staring eyes, the trunk bent with arms clasping and 
embracing the knee and leg of the affected part, is a striking and well known 
picture. Or, the foot is held tenaciously, the sole or dorsum rubbed and 
stroked in fruitless unavailing attempts to mitigate the intensity of the pain. 

So distressing can the symptoms be, that it is little wonder that intense 
mental depression is common. The pain, the disability, the threat of 
gangrene aroused by a knowledge of the fate of fellows in distress, so pervades 
every thought and action of certain cases as to cause complete demoraliza¬ 
tion, and in a few instances has led to attempts at suicide. One of the 
author’s cases successfully accomplished this with illuminating gas; another 
cut his throat with a razor whilst in the hospital, the enormous gash miracu¬ 
lously avoiding the jugulars. 

The author had just made rounds, was called back and was able to save 
the patient by immediate suture of the parts, including the transversely 
cut larynx, and by the introduction of a tracheotomy tube. 


CHAPTER LIV 

THROMBO-ANGIITIS OBLITERANS—VASOMOTOR SYMPTOMS 

What with the perplexing nature of the fleeting pains of the prodromal 
acute stage, what with the long doubtful period of intermittent claudication 
that is so often underestimated or regarded as “rheumatic” or orthostatic, 
and, what with the confusing objective phenomena due to nervous agencies, 
it is little wonder that thrombo-angiitis obliterans is so often mistaken for 
other maladies. The attendant vasomotor disturbances, especially when such 
objectively dominate the clinical picture, may add no negligible onus to the 
clinician’s diagnostic task. Although in thrombo-angiitis obliterans the 
paroxysmal nature of such symptoms is less marked or absent, the coexist¬ 
ence of other neuroses less frequent, the response to emotional influences not 
so striking, there still remain sufficient points of resemblance to account for 
the difficulties of differentiation. 

Vasomotor phenomena may occur independently, unaccompanied by the 
usual hydrostatic and mechanical color changes, at a time when even the 
vessels pulsate, may be superimposed, as it were, or be a coincidental manifes¬ 
tation in a well developed clinical picture of this disease. Both upper and 
lower extremities may be affected. 

It is in the cases of involvement of both lower extremities but with vaso¬ 
motor disturbances confined to one of them, that opportunity for compara¬ 
tive study of the confusing phenomena is afforded. The limb in the more 
advanced stage is usually indubitably stigmatized as the seat of arterial 
occlusion by the ischemia on elevation, chronic erythromelia and pulseless 
vessels. The other limb may be markedly blanched even in the pendent posi- 



272 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


tion—an evidence of vasomotor influence. Such pallor may give way to 
intense cyanosis admixed with areas of an ashen color in which vestiges of 
blanching can be discerned. No rubor develops in this position of the limb. 
The blanching and cyanosis are independent of posture. Persistent syncope 
of short duration followed by cyanosis, uninfluenced by position is one of the 
characteristic types of vasomotor derangement. 

Walking and cold exert a distinct influence in the incitement of neurotic 
vascular manifestations, and the phenomena thus brought forth, have, when 
coupled with the “cramps and pains” in the legs, been described by Erb and 
designated as “intermittent claudication.” We have alluded elsewhere to 
the advantages of segregating the sensory 1 group—which we shall call 
symptoms of “intermittent claudication”—from that of vasomotor insta¬ 
bility, since the two are not necessarily interrelated, mutually dependent nor 
coexistent. 

Referring, here, only to the vasomotor symptoms, it must be recorded 
that transitory or even prolonged syncope may result from either walking or 
exposure to cold in a given case, or from either one of these instrumentalities 
alone. A striking pallor may persist in the pendent position offering a 
marked contrast to the usual hyperemia in this posture, or to the other leg 
if that is also the seat of the malady. The blanching may occupy the whole 
or part of the foot, may spare some of the toes and may be associated with 
patches of cyanosis, the affected area usually presenting a distinct reduction 
in temperature. 

Patients at times will notice very early in the disease that the foot changes 
color. They will say that it has a tendency to become pale in cold weather 
and remain so; in the dependent position, they complain of marked redness 
and often blueness, and at times of coldness. This is a rather constant 
description in many of the histories. Very often these manifestations give 
way to the development of intense local pain in one of the toes with the sub¬ 
sequent appearance of trophic disturbances. Again in some cases, irrespective 
of temperature conditions, syncope and coldness seem to be brought forth 
on exertion or merely on locomotion, the story being “when I go out my 
foot becomes pale; when I take my shoe off, I find it has turned white.” 
To illustrate by a case: 

M. N. examined November 24, 1914. The right foot is very pale, even in the pendent 
position, except for the little toe which is red. When he walks, he says the little toe also 
becomes white. On pressing the toes, the tips become cyanotic. The foot is very cold; 
there are no ulcers and no edema. 

After walking about for a while the right foot again shows signs of vasomotor distur¬ 
bance, but instead of pallor there is a mottling of red and white, there being patches of white 
at the base and over the dorsum of some of the toes, the greater portion of the dorsum 
of the foot being red. At the same time the plantar surfaces of all the toes have a cadaveric 
hue. The right dorsalis pedis and posterior tibial are pulseless; left dorsalis pedis absent, 
but posterior tibial present. 

While an abnormal color may repeatedly afford an unchanging picture 
under similar circumstances, the vasomotor disturbances occasionally exhibit 
a variegation with kaleidoscopic mottlings of tints of yellowish white, red, 
purple and blue. Fugitive pallor may yield to a marmorated combination 
of patches of red and white, these in turn being replaced by cyanotic and 
pallid areas. Or finally, unless a more or less persistent cyanosis ensue, all 
play of colors will cease and reactionary rubor will terminate the ephemeral 
phenomena. 

1 The sensory group has been described in Chap. XLIX on Intermittent Claudication. 


THROMBO-ANGIITIS OBLITERANS—VASOMOTOR SYMPTOMS 273 


Besides the demonstration of one or more pulseless vessels (if such are 
present), and ischemia on elevation, an important and valuable method for 
the recognition of the vasomotor symptoms is the possibility of eliciting the 
phenomenon of reactionary erythromelia. When in doubt, given a case with 
syncope either of spontaneous or induced advent, or with alternating pallor 
and cyanosis, or pallor and patches of red, repeated elevation and depression 
of the leg may dispel all these neurotic displays and produce a distinct and 
continued rubor in the pendent or even in the horizontal position. 

Vasomotor Manifestations May Merely Occupy the Early Clinical Stages of 
the Malady. —Thus, in reviewing the history of a characteristic case (H. R.) 
we find that at a time when the left leg showed all the typical symptoms with 
rubor, the right presented none of these except ischemia on elevation. On 
the other hand, there were vasomotor symptoms in the latter, namely, 
cyanosis, a blanched condition of the foot when the shoe was taken off (par¬ 
ticularly in cold weather), cyanotic patches at the tips of the toes, and cold¬ 
ness. This complex was observed on several occasions. 

Notes taken December i 1908 read: On taking off the left shoe, the foot is fairly red, the 
right is slightly blanched, but all the vessels of the right leg pulsate. However, ischemia 
could be elicited on elevation, an evidence of arterial occlusion. 

If we compare the limb exhibiting vasomotor symptoms with the other 
that is the seat of a more advanced process, we will note that the former is 
not swollen, the toes not tumefied, rubor absent and the color yellowish white; 
or, the toes may be markedly blanched, particularly if they have been exposed 
to cold. In the dependent position, also, a difference is seen in the two 
limbs. The one that combines the early stage of thrombo-angiitis obliterans 
with vasomotor symptoms, shows cyanosis after the leg has been hanging 
down, the distal phalanges or phalanx being of a deep dusky purple; the 
color may be unmixed with any tinge of red, and the rest of the foot also may 
show a cyanotic hue; a pale, ashen skin in many places modifies the picture. 
However, rubor is absent. This condition may change in such a leg, so 
that when the leg is examined 10 or 11 months later (in the case H. R. 11 
months later), the appearance may have completely changed, the usual 
typical signs, marked erythromelia together with or without cyanosis being 
in evidence. 

A study of the case H. R. threw no light on the reason for the marked vasomotor symp¬ 
toms in the right leg. They persisted for a long time. They were present August 17,1908, 
and even November, 1909, at a time when there developed deep cyanosis of the big toe 
due to impending gangrene, and the rest of the foot had a slightly bluish color. The dorsum 
of the foot still exhibited occasional fugitive areas of unexplicable syncope. 

Syncope or Ischemia after Exertion. —While the typical picture of inter¬ 
mittent claudication is characterized by the predominance of sensory mani¬ 
festations sometimes with attendant pallor of the foot and coldness, the 
vasomotor symptoms may exist alone and be evoked by the same form and 
degree of exertion as ordinarily excites sensory responses. One limb may 
be striking because of coldness, the other because of pallor, pain being absent 
in both. The following case will illustrate. 

Thrombo-angiitis Obliterans with Migrating Phlebitis , Syncope and Coldness 
of the Feet after Exertion. 

I. B., Russian, 33 years of age, typical case of thrombo-angiitis obliterans with migrating 
phlebitis states that the right foot becomes white and cold, sometimes pink after walking. 
The left foot also becomes cold and tires easily; the pallor of the right foot is striking, the 
left slightly cyanotic. 

18 


274 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Evidences of Altered Vasomotor Function.—Many as are the clinical 
phenomena illustrative of the peculiar instability of the peripheral vaso- 
motor apparatus, still further evidence thereof is obtainable through simple 
clinical tests. Vagaries in vasomotor function, 1 it is true, may modify and 
impair the uniformity of the demonstrable phenomena; nevertheless, certain 
essentially reliable reactions are wont to follow these motivating factors (i) 
elevation of the limb; (2) thermic influences (cold); (3) mechanical irritation 
(dermatographic reactions); and (4) exercise. 

It has already been shown that all of these may evoke not only immediate, 
but unduly prolonged vasoconstriction of the capillaries and arterioles. 

The vasodilating mechanism may be activated on the other hand through 
such forces as these: Establishment of preliminary ischemia by elevation of 
the leg with consequent refilling of the peripheral vascular branches in the pen¬ 
dent position (reactionary rubor); temporary compression of the femoral 
artery (3 to 5 minutes); or application of a constricting bandage at the root of 
the limb. Less effective means of evoking vasodilatation is the application 
of external heat and diathermy. 

If we examine and compare the healthy and affected lower extremities in 
the horizontal position, we may demonstrate that where there are obstructed 
arteries, normal red dermatographic reactions are usually substituted by 
excessive and persistent pallor; that is, a reversal in the sense of vasocon¬ 
striction takes place over an unusually large zone. The test is thus carried 
out: The femoral artery is compressed for 3 minutes; this is followed by 
tardy and imperfect fading out of the existing chronic rubor of the foot 
(vide Chap. XII, p. 84, paradoxical rubor and ischemia). If then a 
number of scratches be forcibly made over the foot during this period of 
arrested circulation, and the femoral artery be then released, an abnormal 
persistence of pallor in and around the irritated zone will be noted. An 
ischemic area of considerable size will be in striking contrast to the general 
reactionary and intensive rubor of the rest of the foot. 

Quite different will be the reactions of the healthy extremity. Firstly, 
the ischemia of the foot will be more intensive and of more rapid advent after 
the artery is compressed. This paradoxical ischemia on the healthy side has 
been referred to in the Chapter on Collateral Circulation; it is an evidence of 
the lack of development of substituting by-paths where the arteries are patent. 
No such dermatographia alba is here evoked; but the scratches soon attain 
the normal hyperemia. 

Such are some of the demonstrable evidence of altered vasomotility in the 
affected territories. To certain excitants an unusually hypersensitive vaso- 
constricting mechanism is set into motion; to others, vasodilatation. 
Amongst the former agents belong depletion and ischemia (consequent upon 
elevation of the part), cold, mechanical irritation, and exercise. Whatever 
tends to produce a plenum, however, such as the pendent position, sets the 
dilating mechanism into activity. The reactionary rubor in the foot after 
compressing the femoral artery is much more pronounced and of more 
rapid advent on the side of the obstructed arteries—another sign of altered 
vasomotility. 

In explanation of vasomotor lability may be mentioned Kravkof 2 on the effect of throm¬ 
bosis on the vasomotor functions. He states that: “In the coagulation of blood certain 
protein-forming amines are formed, possessing vasoconstrictor powers, and therefore the 
vasoconstrictor effect of the serum may be ascribed, not to adrenalin, but to these protein¬ 
forming amines.” 

1 For vasoneurosis attending arteriosclerotic disease, see p. 578, paragraph 5. 

2 Oppel, Gangraena Arteriitica Suprarenalis, Lancet, July 15, 1922, p. 116. 


TH ROM BO-ANGIITIS OBLITERANS—OSSEOUS CHANGES 


275 


CHAPTER LV 

THROMBO-ANGIITIS OBLITERANS—OSSEOUS CHANGES 

Rather characteristic of thrombo-angiitis obliterans is the absence of bone 
absorption of the terminal phalanges. A differential diagnostic point is 
thus at hand that may serve to distinguish it from Raynaud’s disease and 
sclerodactyly. However, in one case, very marked diffuse bone absorption 



Fig. 48.—General rarefication of the osseous tissue with absence of absorption of the distal 
ends or terminal phalanges in thrombo-angiitis obliterans. 


was noted, involving the lower end of the radius and ulna, all of the carpal bones, 
the bases of the metacarpal, as well as the shafts of the phalanges. The 
radiogram is depicted in Fig. 48. 1 Rarefication of the osseous tissue due 
to impaired circulation and obliteration of the radial and ulnar arteries was 

1 See section Involvement of the Upper Extremities in Thrombo-angiitis Obliterans 
(Chap. LIX). 


276 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


apparently responsible here. But the characteristic disappearance of terminal 
portions of the phalanges was absent. 1 

Secondary destructive osseous alterations, defects, erosions and necroses, 
may occur as the result of trophic disorders, gangrene and infection. But 
these are lesions common to other forms of gangrene, and defective circu¬ 
lation plus infection. 

A diffuse atrophy of bones due to disuse is also no more pathognomic 
than those just mentioned; it may be expected in those in whom one or more 
extremities have been extensively involved or not employed on locomotion for 
a long time. 

A differentiation from the bony changes in the nerve or anesthetic type of 
lepra will be clarified by a reference to Chap. XIV, p. 94. 


CHAPTER LVI 

THROMBO-ANGIITIS OBLITERANS—STATISTICAL DATA 

Although in the light of more recent experiences certain modifications of 
the following data may become necessary, they may be taken as indicating 
average findings in a series of 100 cases collected for special investigation in the 
year 1916. Over 500 cases have come under the notice of the author, but a 
careful statistical review has not been made since 1916. 

Of 100 consecutive cases reviewed, there were 100 Hebrews; of 400 other 
cases observed, 10 Gentiles. 

There were 76 of Russian birth, 17 of Austrian birth, 3 Americans (of 
foreign extraction), 2 Roumanians, 1 German, and 1 Turk. 

The sex incidence was 99 males, 1 female; among the other 400 cases, how¬ 
ever, 2 additional females were studied. 

The division of 100 cases in whom there were 171 lower extremities involved 
was as follows: both lower extremities in 71 cases, the right only in 7 cases, and 
the left only in 22 cases, the preponderance of the left over the right being 
noteworthy. In other words, the majority of cases of thrombo-angiitis 
obliterans, if followed for a sufficiently long period of time, will show the 
lesion in both lower extremities. 

Of the upper extremities, which are less frequently involved, 30 arms 
were affected in 21 cases; both arms in 9 cases, the right only in 5, and the left 
only in 7, again demonstrating a slight increase of the left over the right. 

The cases with involvement of both upper and lower extremities (21) 
revealed involvement of both upper and both lower extremities in 8 cases, 2 
lower and 1 upper in 10 cases, 2 upper and 1 lower in 1 case, and 1 upper and 1 
lower in 2 cases. 

Although the age at the onset of the disease varied considerably, ranging 
from 17 years to 56, the average age was 32 years, 5 months. These figures, 
however, are much too high, since it is very difficult to estimate the exact 
age at which the disease began, because of the insidious nature of the onset, 
and the fact that the onset is overlooked in many cases. 

The advent of gangrene, which in some instances ushered in the disease, 
occurred in others from 1 year and 8 months after the first symptom was 
1 See Chap. XCIX, Raynaud’s Disease. 


TH ROM BO-A NGIITIS OB LI TER A NS—E TIOLOG Y 


277 


noted, to 12 years after the onset. Amputation was carried out in 52 cases 
of the 100. 

In some cases the gangrene set in within a short time or almost simulta¬ 
neously with the apparent onset, the longest period being 12 years after the 
beginning of the complaint. 

Doubtless in many of the cases amputation became necessary at some 
later date, when they were no longer under observation, so that an estimate 
of 75 per cent or 80 per cent would not be too high. 

A similar disease is described as occurring not infrequently amongst the Japanese. 
Koyano collected 120 cases during the years 1900 to 1921, and gives the following deductions. 
Most of the cases occur in young males between the ages of 20 and 40, usually in the labor¬ 
ing classes. Inadequate and poor diet, 1 and local exposure to wet and cold are given as 
factors in etiology. Most of the cases were moderate smokers. The lower extremities were 
most frequently affected. The pulses were extinct in the following order, dorsalis pedis, 
anterior and posterior tibial, popliteal, and lastly the femoral. About two-thirds of the cases 
on admission to the hospital had already lost the right and left popliteal pulses. The blood 
viscosity was somewhat high, 5.16 in the average case (Koyano); blood sugar normal, as 
well as cholesterol. The Wassermann test was usually negative. The Japanese laud con¬ 
siderably the hypodermic injections of Ringer’s solution (Mayesima-Koga), attributing’its 
efficacy (?) to its power to diminish the viscosity of the blood. The same author was able 
to find the “acute” lesions in but one case, and therefore is surprised at the relative 
frequency of the characteristic findings amongst the cases observed in the United States. 
Evidently the migrating phlebitis was either overlooked or it is rarely associated in the 
disease of the Japanese. 


CHAPTER LYII 

THROMBO -ANGIITIS OBLITERANS—ETIOLOGY 

The cause of the pathological process in thrombo-angiitis obliterans has 
not yet been definitely established. By his studies of the clinical aspect 
and pathology of the disease, the author has established the following facts. 
That the disease is not an endarteritis obliterans; that it is an occlusive 
thrombotic process involving the deep arteries and veins of the upper and 
lower extremities, or the superficial veins; that the early stages of the dis¬ 
ease manifest themselves in an inflammatory lesion which shows a specific 
and characteristic morphological picture, while in the process of healing; 
and that in the early or acute stage, certain purulent foci make their appear¬ 
ance that would suggest a microbial agent or infectious causative factor. 
No organism, however, has a yet been demonstrated, even in the superficial 
veins, when these are in the stage of acute inflammation. 

Syphilis has been regarded by some as a possible cause, but a study of 
the histories and of the Wassarmann tests in more than 30 cases 2 has shown 
that lues is not responsible. 

It is a striking circumstance that of a series of 500 cases, the author found 
only 3 cases in women, and in these patients no amputation was performed, 
so that the diagnosis was made on clinical signs alone. Furthermore, it is 
interesting that but 4 cases out of 500 did not belong to the Semitic race. 

1 Some of the more intelligent Russian immigrants have called the author’s attention to 
this factor; but this is irreconcilable with the development of the malady in cases in affluent 
circumstances since birth. 

2 Buerger and Kaliski, Med. Rec., Oct. 15, 1910. 


278 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Tobacco is probably a predisposing factor, and may be regarded at least 
as causing some alteration in the vessels that makes them liable to the attacks 
of inflammation and thrombosis. Most of the cases are heavy smokers, 
although smoking was denied in i per cent of the author’s cases. 

Here, more especially than in any of the organs or tissues of the body, 
must we seek not only for predisposing moments, but also for the agency 
that directly motivates the inflammatory thrombotic lesion. The conducive 
factor can certainly not be held wholly accountable. Unwarrantable are 
inferential hypotheses that would attribute an essential role to mere con¬ 
tributory forces. It is immaterial whether these be ontogenetic (individual¬ 
istic traits) or phylogenetic (Hebrew races), acquired (as thermic cold), 
traumatic (after cutting nail, etc.), inebriant or chemical intoxicants (nico¬ 
tine, ergot, toxins of typhus). 

An understanding of the histological alterations in the vessels could limit 
the promulgation of hypotheses or etiology that are of purely theoretical 
nature. 

Predisposition to Thrombosis .—If a bland thrombosis without inflamma¬ 
tory process occurred here, we could perhaps have greater confidence in 
those hypotheses that seek a special thrombophilic tendency in explanation 
of the extensive obturating process. Although a certain chemical predisposi¬ 
tion of the intima or a diminished metabolism in the vascular wall (Zurhelle 1 ) 
cannot be excluded from the realm of possibility and may lend to the blood a 
tendency to clot in loco, it is more likely that the determining factor is that 
sum of chemical and toxic moments that are set into activity pari passu with 
the incidence of the inflammatory lesion. 

From time to time most interesting explanations are given by various 
authors and commentators of the cause of this malady, and often individual 
predisposing factors are dignified by the appellation “ exciting cause.” Thus, 
hyperglycemia, or an increased sugar content of the blood, and dyscra- 
sias of endocrine origin have been suggested as causative factors (W. Meyer). 
But we must not forget that enough clinical and pathological data are at 
hand to furnish us with a reliable concept as to what is here actually influen¬ 
tial in producing the changes in the vascular system. It is known that the 
arteries and veins, par excellence, furnish examples of tissue complexes 
requiring several factors for production of pathological alterations. And, 
strange to say, one or another of these factors (that are merely predisposing 
agents) are apt to be singled out and heralded as the true cause. When 
the author’s pathological studies revealed that certain specific histological, 
architectural alterations in the vessels were characteristic of the disease 
thrombo-angiitis obliterans, it was not presumptious to conclude that 
a special exciting agent, be it a toxin or organism' must play a role here, in 
addition to the many other conducive circumstances that may play larger or 
smaller parts. For how else can we explain the occurrence of the unique or 
specific alterations that are found nowhere else in thrombotic processes and 
are a pathognomonic for thrombo-angiitis obliterans, just as the peculiar 
pathological pictures of tuberculosis are attributable to the tubercle bacillus, 
and the changes seen in the glands of Hodgkin’s disease are doubtless the 
reactions to special agents. 

Reverting to the peculiar reaction of arteries and veins, one may empha¬ 
size the fact that more than one factor must be invoked in the case of these 
peculiar tissue changes. Thus, stasis, locomotion, dependency of the limbs, 

1 Zurhelle, Zentralbl. f. Gynec., 1908, No. 43. 


THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 279 


activity of circulation, vis a tergo, tobacco, age, sex, and thermal influences 
—all these play greater or lesser roles in determining thrombotic and athero¬ 
matous occlusion. 

As for tobacco, its influence has been recognized for many years. Erb, 
long ago, in papers written subsequent to his publications on intermittent 
claudication, attributed extensive atherosclerotic conditions of the lower 
extremities, in the main, to the influence of tobacco. Just how far the absorp¬ 
tion of tobacco poisons is responsible for the degenerative changes in the 
arterial walls cannot be determined accurately, but that it may be safely 
regarded as a predisposing cause, no one will venture to deny. So also in 
thrombo-angiitis obliterans, it is possible that the use of tobacco may render 
the vessels more susceptible to special agents, be they toxic or infectious, but 
that tobacco is the only and exciting cause is exceedingly doubtful and highly 
improbable. 

Cases of migrating phlebitis in patients who are heavy smokers occur not 
infrequently. In these, the territory of the saphenous vein becomes 
gradually occluded, and the differential diagnosis between migrating phlebitis 
of the “bland type” and migrating phlebitis associated with thrombo-angiitis 
obliterans must be made. If we exsect a portion of the vein in thrombo¬ 
phlebitis of the bland type, we find, it is true, slight changes in the media, 
but an occlusive thrombus that presents none of the characteristic lesions. 
In such cases we are dealing with a bland thrombosis in vessels that are 
damaged by various influences, tobacco, or other causes. In thrombo¬ 
angiitis, however, when migrating phlebitis occurs, certain specific architectural 
changes can regularly be diagnosticated and found under the microscope. An 
infectious agent is in all probability, responsible for the “acute” or earliest 
lesions. The evidences in favor of this view are discussed at length else¬ 
where. 1 It is of some interest to note that persistent leukocytosis has been 
observed in the early stages of this malady (Thomas 2 ). In a case of extensive 
vascular occlusion of doubtful origin 3 (obliterating thrombo-arteritis, possibly 
thrombo-angiitis obliterans) leukocytosis was present for a number of months. 
That something else must call forth or evoke such remarkable architectural 
complexes seems unquestionably true. 


CHAPTER LVIII 

THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 

There is no phenomenon of more importance in elucidating the true nature 
of the pathology of thrombo-angiitis obliterans than the characteristic 
thrombo-phlebitis or “migrating phlebitis” of this disease. The asso¬ 
ciation of thrombosis of superficial veins of the upper and lower extremities 
with other evidences of obliteration of the larger arteries occurs in a 
sufficiently large number of cases to make the affection of the veins almost 
pathognomonic^ 

Pathology of the Acute Stage, Chap. LXI. 

2 Thomas, Am. Jour. Med. Sc., 165, Jan., 1923, p. 86. 

3 P. 474, Case G. G. 


280 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Those interested in a more intensive and comprehensive study of this 
disease will find a critical review of the clinical history of such cases of great 
value. 

For the sake of clearness the cases of thrombo-angiitis obliterans attended 
with thrombo-phlebitis or migrating phlebitis may be divided into seven 
different groups, (i) Cases of thrombo-phlebitis without symptoms. (2) 
Thrombo-phlebitis with symptoms of limited vein involvement. (3) Migrat¬ 
ing phlebitis causing the patient to seek treatment. (4) Cases in which both 
the migrating phlebitis and thrombo-angiitis obliterans play equally important 
roles in the symptom-complex. (5) Migrating phlebitis involving both the 
upper and lower extremities. (6) Extensive migrating phlebitis of the 
chronic fulminating variety associated with a similar process in the deep and 
femoral veins; and (7) migrating phlebitis with a long prodromal phase, 
evidences of deep arterial involvement being lacking over an extended period 
of time. 


I. THROMBO-PHLEBITIS WITHOUT SYMPTOMS 

There are patients who have no knowledge of the occurrence of any 
trouble in the veins of the leg, but in whose amputated limbs extensive old, 
or old and recent thrombo-phlebitis of the internal saphenous or its tributaries 
is discovered. Such a case was J. C., who could recall nothing referable to a 
disturbance in the superficial veins. Study of the vessels revealed old occlu¬ 
sion of a large part of the saphena by virtue of a thrombotic process, and some 
areas of more recent thrombo-phlebitis. Sometimes an augmented streak 
corresponding to the course of the internal saphenous with induration under 
it, may be a definite evidence of a healed thrombotic lesion in the 
corresponding vein. 

Case 1. J. C., 45 years, Russian Hebrew, admitted May 18, 1908; has eight children 
(all well); gives a rather typical history of vascular disease of both lower extremities, 
resulting in amputation of the left leg at the knee. Four years ago he had “rheumatism” 
of the right leg with pain in the sole of the foot and redness of the toes lasting eight months. 
Since then it has not troubled him. The left leg, however, began to hurt him last summer; 
he could not walk a block without taking a rest. His big toe became “sore” recently, 
and now the pain in the foot is constant. He is told that the big toe is becoming gangre¬ 
nous, and that his leg should be amputated, which he gladly permits. 

With the observation just cited, no new clinical facts are adduced, but 
certain similarities between the thrombotic lesions of the saphenous vein, 
as seen under the microscope, and the changes characteristic of the closed 
deep vessels were deemed sufficiently suggestive to warrant the suspicion 
that here, in the superficial veins, a new territory for the process “ thrombo¬ 
angiitis obliterans” had been found. 

II. THROMBO-PHLEBITIS WITH SYMPTOMS OF LIMITED VEIN 
INVOLVEMENT 

A more interesting group is represented in those patients who come to us 
with active thrombo-phlebitis and periphlebitic manifestations. Here and 
there along the course of the internal or external saphenous vein, alterations 
in the skin and subcutaneous tissues occur. These are in the form of small, 
erythematous, slightly indurated patches, about a centimeter in diameter, 
and tender to the touch. Were it not for the concomitant phenomena refer¬ 
able to the tributaries of the saphenous or the trunk itself, the nature of these 
cutaneous nodosities would have remained obscure. With the appearance 


THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 281 


of these, however, or at other times in the course of the disease, cord-like 
thickenings of portions of the long saphenous, with or without adhesion to 
the skin, are frequently observed. As examples let us briefly tell the story 
of Cases 2 and 3 in Group II. 

Case 2. S. S., 30 years old, Russian Hebrew, admitted July 8, 1907; father of one child; 
has been suffering for four years with “weak legs;” for two years there has been pain in his 
left foot. About one and one-half years ago the second toe became gangrenous and was 
removed. Last winter his attention was directed to the blueness of the toes; it was difficult 
to keep the left foot warm. For a couple of years he has noticed that u red spots” come and go 
along the inner and outer side of the shin hone. They are a little painful and disappear with¬ 
out treatment. Now he seeks advice because the little toe looks as if it were going to die off. 
Amputation just above the middle of the leg. 

Diagnosis .—A typical case of thrombo-angiitis obliterans with gangrene of the little toe 
of the left leg and cutaneous nodosities along the course of the internal saphenous vein from 
the ankle up Jo the region of the tubercle of the tibia; probably closure of a part of the 
saphenous vein. 

The study of the vessels of the amputated leg showed extensive occlusion of the posterior 
tibial, anterior tibial, peroneal, and plantar arteries (thrombo-angiitis obliterans). The 
long saphenous vein was filled for the most part with old organized tissue of a type indis¬ 
tinguishable from that seen in the deep vessels, and some of its tributaries were closed by 
more recent obturating masses. The cutaneous nodules correspond to the distribution of 
the finer tributaries, but inasmuch as they had almost completely disappeared at the time of 
operation, no histological examinations were made. 

As representative of the occurrence of migrating thrombo-phlebitis of 
the long saphenous and of erythematous nodosities in the same patient, let us 
cite Case 3, who observed and related quite accurately how the painful 
“ hard cords ” developed. 

Case 3. F. S., 37 years old, Russian Hebrew, father of two healthy children, April 13, 
1909; says that he remembers having had peculiar pains in the soles of both feet on walking 
a few blocks for the last three or four years. About four months ago the big toe began to 
trouble him, but even before that he noticed hard cords along the inner side of the leg. Since 
then the nail of the big toe came off, leaving a raw wound which refuses to heal. The long, 
hard strands come and go; sometimes they are seen high up on the leg; at others, three or 
four inches above the ankle. Besides this there are lumps farther hack on the inner side of the 
leg. Patient does not return for treatment, so that the further course of the disease is 
unknown. 

On physical examination the usual signs of thrombo-angiitis were found, with a trophic 
ulcer of the big toe. There were no evidences of recent thrombosis of the long saphenous 
other than one hard node four inches above the ankle; evidently the last attack of thrombo¬ 
phlebitis had subsided. The other leg showed somewhat less advanced symptoms of the 
disease. 

Here, then, we are dealing with a case in which both the patient’s 
narrative and ocular evidence point to the association of superficial and 
deep thromboses. 

III. MIGRATING PHLEBITIS CAUSING THE PATIENT TO SEEK TREATMENT 

When the attacks of migrating phlebitis make their appearance early in 
the history of the case, and when the attendant discomfort and pain are 
sufficiently great, then the symptoms belonging to the true, deep-rooted 
affection— thrombo-angiitis obliterans —are sometimes wholly ignored by the 
patient and remain undiscovered by the physician^ Medical advice is 
sought only for the “lumps” and “hard, tender strands” or “cords” that 
are oftentimes so disturbing. Such observations are of no mean importance 
in diagnosis, since they have taught the author to seek for the early subjective 
and objective signs of thrombo-angiitis in every patient in whom there are spon¬ 
taneous and unaccountable attacks of inflammation of superficial veins. Let us 


282 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


see what we can learn, then, from Group III, in which migrating phlebitis 
causes the patient to seek treatment. 

Case 4. E. B., 36 years old, Austrian Hebrew, consulted me on January 17,1909, with 
the history of having had stinging sensations on the inner side of the right leg, low down, 
some three months previously. A few days after the onset of this trouble he could feel a 
long, thickened “lump” behind the shin bone, a short distance above the ankle. Soon after 
this, another swelling, not unlike a “hard cord,” appeared somewhat higher up on the leg, 
was very tender, and was succeeded not many days later by a third somewhat shorter 
strand. 

Upon close questioning he admitted that although he seeks relief from the symptoms 
mentioned, he has been annoyed for almost a month before the beginning of the present 
affection by frequent cramp-like pains in the calf of the right leg upon walking a few (five or 
six) blocks. 

Physical examination, January 17, 1909, revealed induration of the tissues about the 
saphenous vein, from the ankle to the upper fourth of the leg. The distal portion presents 
a cord-like thickening, with scarcely any inflammatory signs. Higher up, however, the 
skin is adherent to the deeper hardened area, and is exceedingly tender to the touch. 

The dorsalis pedis and posterior tibial arteries of both legs are pulseless; the femorals and 
popliteals can easily be felt to beat. The big toe of the right foot has a cyanotic hue. 

Course. —January 31, his phlebitis was found much improved; his right big toe often 
hurts him, and his foot easily gets “cold” and “tired.” 

Two months later, March, 1909, no evidences of the old thrombo-phlebitis can be found. 
The big toe of the right foot still shows a peculiar bluish discoloration, and the absence of 
pulsation in the vessels is the same as before. There are no trophic disorders; the most 
striking phenenomon is the vasomotor disturbance in the big toe. 

In short, we have here an exquisite example of a combination of early 
manifestations of thrombo-angiitis obliterans (pain on walking, evidences of 
disturbed ciculation), with attacks of thrombo-phlebitis in the territory of 
one of the saphenous veins. 

Whereas pathologic proof of the correctness of the diagnosis—thrombo¬ 
angiitis obliterans—is lacking in the last case, the history of another patient 
will be given in whom there were similar symptoms, and in whose amputated 
limb and exsected veins ample material for anatomical investigation was 
found. 

Case 5. M. K., 44 years, Russian Hebrew, father of three healthy children, was 
admitted to the hospital on December 8, 1908. His limbs never troubled him until 
about a year ago, when he felt the presence of tender spots on the inner side of the right foot. 
Soon other hard “lumps” and “cords” appeared, some of these in the neighborhood of the 
ankle, others higher up on the leg. After two months these disappeared, only to recur after 
a very short interval. Since then he has never been absolutely free from peculiar “painful 
spots,” and now, on admission, he still has signs of some of them. About three months 
after the onset of these symptoms he experienced pain in the big toe, especially on walking. 
This has become gradually worse, so that he has been unable to get about properly for 
almost two months. Of late he has often had cramps in the calf and instep of the right leg 
after walking for a short distance. His chief complaint, however, is the painful condition of 
the inner side of his right leg. 

Physical examination showed evidences of circulatory disturbance in the right lower 
extremity. Both the dorsalis pedis artery and the posterior tibial were pulseless, although 
pulsation of both the femoral and popliteal arteries could be easily detected. 

Over the inner border of the right foot there is a red streak about one-half inch in length. 
This corresponds to a tender indurated mass which thins out and is lost as it is traced 
upward. A short distance below the middle of the leg the upper end of a hard cord can be 
palpated. This extends down behind the border of the tibia for more than two inches, is 
adherent to the skin, somewhat nodulated, and marks the center of an area of hypersensi¬ 
tive, swollen, turgid skin. There are no trophic disturbances. Diagnosis — thrombo¬ 
angiitis, and thrombo-phlebitis of the internal saphenous and some of its tributaries. 

On December 15, 1908, a portion of the thrombosed saphenous was removed for patho¬ 
logical examination. 

On December 26, 1908, the physical examination was recorded as follows: In the hori¬ 
zontal position the right foot has a light shade of red; this is most marked over the big toe, 
and fades off towards the ankle. In the web between the third and fourth toes there is a 


TH ROM BO-A NGIITIS OBLITERA NS—MIGRA TING PHLEBITIS 283 


superficial ulcer. On the inner side of the foot, almost two inches from the internal malleo¬ 
lus, there is a hard, cord-like nodule which is adherent to the skin. Behind the tibia there 
is a scar left after removal of a portion of the saphenous vein. The saphenous vein can no 
longer be felt. 

On elevation of the foot, blanching sets in rapidly and pain becomes intense. The 
pendent foot turns very red (marked erythromelia). 

Further Course.—February 15, 1909, the pain in the foot has been getting steadily 
worse, and the fourth toe is beginning to turn black. On the 23d of February amputation 
at the knee was done, at the request of the patient, for early gangrene of the fourth toe. 

The prognostication that was made clinically in regard to the condition of 
the long saphenous vein was confirmed by pathological examination of the limb 
for, practically the whole of the main trunk of this vessel was found converted 
into a fibrous cord, the result of an old thrombotic lesion, similar to that found 
in the deep vessels. As for the arteries, the plantars, peroneal, posterior 
tibial, and lowermost portion of the popliteal were completely occluded by the 
brownish organized tissue usually encountered in the disease under con¬ 
sideration, whilst the deep veins were patent throughout. 

Stated succinctly the case is one of thrombo-angiitis obliterans, in which 
the symptoms manifested themselves first in the form of migrating phlebitis 
that has persisted almost the whole of the years’ course of the disease. The 
thrombotic lesion has affected the right leg and is associated with the develop¬ 
ment of typical symptoms of thrombo-angiitis. At the end of the year some 
of the deep vessels are closed, for there is absence of pulsation in the dorsalis 
pedis and posterior tibial. For a long time there are no trophic distur¬ 
bances, but finally in the thirteenth and fourteenth months of the disease, 
ulcers develop and dry gangrene of one toe leads to amputation of the limb. 

When the migrating phlebitis is a prodromal manifestation of the disease, 
thrombo-angiitis obliterans, or, if it marks a relapse in an apparently healed 
case, no phenomena referable to obliteration of the deep vessels may be obtain¬ 
able. In such instances the excision of the affected superficial vein, followed 
by microscopic examination, will frequently reveal the typical pathognomonic 
lesions upon which a correct diagnosis may be based. 

Case 6. H. P., 42 years, Russian Hebrew, seeks advice for a hard lump in back of the 
left leg on November 15, 1912. Twenty years ago the tip of the big toe of the right foot 
was removed in Russia, ostensibly for frost-bite. Since then (the exact date being unknown) 
the second toe of the same foot was also ablated. Save for these affections, no symptoms 
referable to the extremities can be recalled by the patient. 

Physical examination shows a small thrombosed nodule, apparently associated with a 
varicose vein, over the calf of the left leg. In the vicinity there are small nodules, seemingly 
connected with tributaries of the external saphenous. There are no evidences of closure 
of the peripheral vessels. 

Histological examination of the excised nodule, December 7, revealed the typical lesions 
of thrombo-angiitis obliterans. 

Summary .—We have here, then, a case in which the history of the loss of two toes points 
to the existence of an old-standing thrombo-angiitis obliterans, the disease having become 
spontaneously cured. Recently there have developed evidences of involvement of super¬ 
ficial veins, the histological studies corroborating the diagnosis. 

Another striking instance of the cases in which the thrombo-angiitis 
obliterans symptoms are masked and not noticed by the patient, and where the 
patient seeks advice because of migrating phlebitis, is presented by the 
following case: 

Case 7. J. W., Russian Hebrew, consulted the author in November, 1911, because of 
red lumps in the left leg, and indefinite pains. He thinks he had syphilis 16 years ago, and 
that the lumps now present are due to this disease. The present trouble dates back about 
six weeks. 

Physical examination shows a number of nodules of the usual type over the outer and 
posterior aspects of the left leg, and along the course of the internal saphenous vein. 


284 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


On November 26, one of these nodules was removed for microscopic examination. 
Pathological examination shows the typical lesions of thrombo-angiitis obliterans in the 
early stages, typical giant cells, and miliary foci. Wassermann reaction on the 26th of 
November was negative. 

December 4, some of the nodules had disappeared completely. The internal saphenous 
vein can be felt as a hard cord one-half way up the leg. 

February 16, 1912, a fresh nodule has appeared above the Achilles tendon, another over 
the left calf, still another over the outer side of the leg above the external malleolus. 

The dorsalis pedis and posterior tibial vessels of the right leg pulsate. The dorsalis 
pedis of the left does not pulsate. The posterior tibial pulsates very faintly. 

We may cite as exemplifying cases of this group, the following history. 

Case 8. B. C., 39 years, Russian Hebrew, seeks advice on account of pain in the left 
leg, which came on about four months ago. This seems to be associated with a nodule on 
the inner side of the middle of the tibia, and a similar nodule somewhat lower down. Three 
weeks ago another lump appeared on the outer aspect of the right leg. He has no pain on 
walking, and none of the symptoms of thrombo-angiitis obliterans. 

Physical examination, December, 1911; several typical phlebitic nodules over the inner 
aspect of the left leg. The internal saphenous vein, from a point just above the ankle up 
to the upper fifth of the leg, can be felt as a hard cord. Anteriorly, three inches above the 
ankle there are two fused nodules in a somewhat reddened skin. 

The dorsalis pedis and posterior tibial arteries are not felt in the left leg. The posterior 
tibial pulse of the right leg is also imperceptible, though the dorsalis pedis pulsates faintly. 
There is no erythromelia, but moderate ischemia on elevation of both limbs. 

In short, we have here a case in which the symptoms of migrating phlebitis are promi¬ 
nent, the pulseless vessels and slight ischemia being the only evidences of thrombo-angiitis 
obliterans. 

On December 5 one of the nodules was removed from the left leg for microscopic 
examination. 

December 16. The phlebitis is extending from the region of the excised nodule in the 
upper part of the leg, and a distinctly tender cord, some inches long can be felt along the 
course of the saphenous. 

December 22. The nodules in the right leg have almost disappeared. 

Still more interesting and instructive are those cases in which the disease 
of the superficial vessels affects both legs and one or both thighs. 


IV. BOTH MIGRATING PHLEBITIS AND THROMBO-ANGIITIS PLAY 
EQUALLY IMPORTANT ROLES IN THE SYMPTOM-COMPLEX 

The following case will illustrate this variety. The patient could be 
observed for almost a year, the progression of the obstructive changes in 
the deep vessels could be closely followed by proper interpretation of the 
varying circulatory phenomena in the leg, and many of the attacks of 
thrombo-phlebitis in the territory of at least one saphenous vein could be 
recorded. 

Case 9. H. R., 32 years, Russian Hebrew, August 9, 1908, has been suffering for five 
years. At first it was a burning sensation in the toes of the left foot that gave him most 
concern, but later on he was troubled more by his inability to walk distances on account of 
the sudden advent of attacks of pain that were felt from the toes upward almost to the knee. 
In cold weather he seems to be in poorest condition, for then his toes get cold and blue, and 
walking is very difficult. Although this has been going on for years, he has not found it 
necessary to consult a physician until something else in his right leg began to engage his 
attention. 

For the last five months long “streaks” or “swollen places” would come and go over 
the inner side of the right leg, behind the shin bone. These are often very painful. A week 
ago a physician told him that he had “phlebitis.” 

Physical examination on August 17, 1908. The vessels of the right leg pulsate, but the 
left posterior tibial and dorsalis pedis cannot be felt. 

The right leg shows a tender cord with some edema around it, extending from the ankle 
almost to the tibial tubercle. This corresponds to the long saphenous. Erythromelia is 


TH ROM BO-A NGIITIS OBLITERA NS—MIGRA TING PHLEBITIS 285 


definite on the left side, there are no trophic disturbances, and the circulation of the right 
leg is fairly good. 

From now on aggravation of his subjective condition went hand in hand with the 
advancing lesions in the vessels. That an increase in the extent of vascular occlusion took 
place from this time on could be easily deduced from clinical observation. 

On December i, 1908, the following was recorded: The right foot looks pale (evidence 
of the beginning of circulatory disturbances). After a short time it becomes slightly cya¬ 
notic. If looks cadaveric when raised for a short time. There is no erythromelia. The 
dorsalis pedis does not pulsate. A tributary of the long saphenous about two inches long 
can be palpated as a tender cord along the lower inner aspect of the right thigh; the skin 
over it is reddened. There are two nodosities in and under the skin below and to the inner 
side of the tubercle of the tibia. The left leg shows marked erythromelia; blanching in the 
elevated position is extreme; the popliteal is open, but the dorsalis pedis and posterior tibial 
arteries cannot be felt. There are no ulcers or other signs of trophic disorder. 

The steady advance of the occlusive process in the deep vessels is well 
illustrated by the findings on December 1, 1908. In August all the vessels 
of the right lower extremity pulsated in normal fashion; now, in December, 
the dorsalis pedis is occluded. Corresponding with this there is a new symp¬ 
tom, the blanching of the foot. How remarkable that the disease of the 
deep vessels on the right side should be so closely associated with the attack 
of migrating phlebitis, the latter first attacking the saphenous in the leg, and 
now appearing in the thigh! We have evidences of chronicity in the affection 
of the superficial veins, and as regards the deep lesion, we have been able to 
watch its gradual development both by its effect on the palpable arteries and 
by the clinical manifestations it has produced. 

On January 31 the big toe of the left foot was swollen and red; the nail was coming off. 
Immediately upon removing his shoe, the right foot had a very white color, but soon 
cyanotic patches mingled with the pallor all over the foot, especially in the region of the big 
toe. The pain in the left foot was now excruciating and he consented to an amputation 
with scarcely any reluctance. The left leg was amputated at the upper fourth. 

Examination of the vessels of the amputated limb showed occlusion of the following 
arteries: Dorsalis pedis, peroneal, plantars, and posterior tibial. The anterior tibial artery 
was open throughout most of its course. A large part of the long saphenous vein was found 
occluded by an organizing thrombotic process. 

Diagnosis. —Thrombo-angiitis obliterans. 

In short, this patient presents the following features of interest: (1) 
Migrating thrombo-phlebitis of both saphenous veins; (2) involvement of the 
same vein in its course through the thigh; (3) associated progressive and 
synchronous development of the thrombosis in the superficial and deep vessels 
of the right lower extremity; and (4) absence of any cause for the lesion of 
the superficial vessels. 

Case 11. W. T., 26 years, Russian Hebrew, admitted July 10, 1909. 

In April, 1907, he was treated for gangrene of the third toe of the left foot. Three 
months before admission to the hospital he had been suffering with pain in the left calf and 
foot. During the previous winter (1906) the left foot did not seem to be normal, so that he 
sought the advice of an orthopedist, who gave him the usual treatment for flat feet. Lat¬ 
terly, he has had severe pain in the calf, and shortly before admission gangrene of the third 
toe set in. He had an amputation performed on the 27th of May, 1907, the left leg having 
been ablated at its upper third. 

At that time pathological studies revealed the usual changes that are seen with thrombo¬ 
angiitis obliterans. The dorsalis pedis, posterior tibial, the greater portion of the peroneal 
and plantar arteries were closed. 

Present Status (1909).—Since discharge, June 27,1907, until eight months ago, he seemed 
to be doing well. About this time (8 months ago) he noticed the appearance of red streaks 
and iiodules on the inner side of the right thigh. After a few days these would disappear 
and new ones would appear in their stead, either higher up on the thigh, or near the knee. 
They caused a peculiar pricking sensation, and some were tender and painful. Lately, he 
has been able to walk no more than two hundred steps without resting. 


286 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The external manifestations on the ioth of July, 1909, were as follows: 

A healed amputation scar in the left leg. In the dependent position there is marked 
erythromelia of the right leg. Neither the dorsalis pedis nor the posterior tibial can be felt 
to pulsate. On the inner side of the thigh, near its middle, there is a sensitive strand, which 
corresponds to the thrombosed saphenous vein. On the outer side there are a number of 
hard, indurated, reddened nodules. Over the inner side of the dorsum of the foot there are 
similar nodules and strands. 

Diagnosis .—Migrating phlebitis and thrombo-angiitis obliterans. 

In short, the history of this case reveals the following: Thrombo-angiitis 
obliterans first involving the left lower extremity, leading to amputation; 
insidious development of the same disease in the right lower extremity, with 
extensive thrombosis of the superficial veins of the thigh and leg. 

From the consideration of the data thus far presented it would appear that 
the internal saphenous vein is the site of predilection for that peculiar lesion 
which is termed a migrating phlebitis. In July, 1904, the author had the 
opportunity of studying a case in which the veins of the upper extremity, 
too, were involved. Since then several additional patients with a similar 
distribution of the lesions have come under observation. 


V. MIGRATING PHLEBITIS OR THROMBO-PHLEBITIS INVOLVING BOTH 
UPPER AND LOWER EXTREMITIES 

In three out of four of these patients the disease has reached that stage of 
chronicity in which the suffering is almost constant and in which the limbs 
may be regarded as irretrievably lost. For there are cases that become ‘‘ cured ’’ 
as far as symptoms are concerned. And by “cured” in this sense we do not 
mean to imply that the pulseless dorsalis pedis, posterior tibial, or both, 
begin to beat again, but rather that, in spite of closed vessels, an adequate 
collateral circulation has become established, as evidenced both by the 
absence of the typical manifestations of impaired circulation, and by the 
patient’s improved subjective state. These three patients per contra had the 
“severe” form of the disease, even though the issue, gangrene, was delayed 
far beyond our expectations. 

Case 11. B. B., 34 years, Russian Hebrew, married, has no children; operator for 
eleven years. His malady began eight years ago, when he first experienced pain in the right 
calf on walking. He would be compelled to rest hfter walking four or five blocks. At about 
the same time he often noticed that there were long “hard cords” and “reddened lumps” 
over the front of both forearms (anteriorly) and over both legs. These would come and go, 
appear with provocation, now in an arm, now in a leg. The lumps were always small, 
pea-sized or slightly larger, and could be felt for two or three days. 

He always felt better during the summer months. The nodules in the legs were present 
almost every winter for the first five years. Six years ago there was a “ bad attack,” in the 
course of which there were (“Adern”) “veins” or “nodules” behind and above the right 
ankle. Then again, about three years ago, there was a repetition of this trouble. Nodosi¬ 
ties formed behind the shin bone on the inner side of the right leg (region of saphenous) and 
the pain kept him abed for almost ten weeks. 

Thus, up to this time he complained of the following: Pain in the right calf on walking 
two to four blocks, painful nodules and cords, and cramps in the toes and sole of the right 
foot at night. 

For two years the left leg has given him concern; the condition is practically the same as 
that of the right. Last winter, January, 1909, there were “sores”—one at the tip of the 
big toe of the left leg, and another at the end of the little toe of the right. He feels best 
when his legs hang down (a variation from the usual statement); but even in this position 
the toes often feel “dead.” In the same way his fingers get “numb” in winter; he thinks 
that there is no blood in them. 

Physical Examination. —In the right leg the toes have a tense, reddened appearance, 
the second and third being discolored most, the little toe having a cyanotic hue. Just behind 


THROMBO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 287 


the nail on the plantar surface there is a deep fissure, the tips of which are adherent. Slight 
pressure brings forth a drop of pus from the bottom of the wound. The erythromelia is 
marked over the dorsum of the foot, as well as over the sole. Ischemia in the elevated 
position is intense; this posture excites severe pain. The femoral artery pulsates* the 
popliteal, posterior tibial, and dorsalis pedis cannot be felt. 

The left leg is similarly affected; the rubor is deeper and the toes are more swollen. 
There is a trophic ulcer at the tip of the big toe. The ischemia, too, is of a greater degree 
All the vessels (femoral included) fail to pulsate. 

Summary. —This is a case which, according to the story, combines 
thrombo-angiitis obliterans with migrating phlebitis of both upper and lower 
extremities. 

One of the most instructive cases of this series is a patient in whom the 
attacks of inflammation and thrombosis of superficial veins dominated the 
clinical course for years before the symptoms characteristic of thrombo-angiitis 
obliterans came into evidence. 

Case 12. D. B., 35 years, Russian Hebrew, first seen by the author July 16, 1904 
He had been treated in the hospital eight years previously for “phlebitis” of the right 
leg; a portion (5 inches) of a large vein was diseased at that time, and the history states that 
the process was “migrating,” moving up and down the thigh. He says that this trouble 
lasted off and on for two years. In 1903 there were “lumps” in and under the skin of 
the right leg, and then, three months later, in the left leg. Such swellings would last a 
week, develop into hard “tender spots” with a covering of red skin, and on one occasion 
three such spots appeared on the left arm, in front of and just below the elbow. 

Physical examination , July, 1904. In the left antecubital region there is a thickened, 
slightly reddened cord about two inches long. Another is situated on the ulnar aspect of 
the same forearm, near the elbow. The right forearm presents a similar vein about three 
inches from the elbow; the skin is not reddened. On the inner side of the right cubital 
space a subcutaneous adherent nodule can be felt; it is very tender. There are several 
such nodules in the right calf and smaller ones over the left shin bone. No edema, but 
slight cyanosis of both legs in the pendent position. A portion of one of the thrombosed 
arm veins was extirpated for study. 

Course .—A year later, 1905, symptoms referable to affection of the deep vessels of the 
left lower extremity manifested themselves, to wit: Coldness and blueness of the left foot 
and superficial ulcers on the toes. 

Thus far our patient presented no striking addition to the symptom-complex under 
discussion, other than the thrombo-phlebitis of the arm veins. In 1907, however, he devel¬ 
oped a gangrenous patch at the tip of the middle finger of the right hand. This rather 
unique site for trophic manifestations is rarely seen in obliterating thrombo-angiitis, and 
therefore deserves more detailed mention. 

February 1, 1907, D. B. stated that his doctor had been treating him for a “felon” 
of the middle finger of the right hand. His hand had been cold for several weeks, and the 
middle finger was painful. Four weeks previously a black “ dead ” spot formed on the tip 
of the finger, and since then, what with cutting it and self-treatment, he thought that the 
present intensely painful affection had overtaken him. 

Physical examination,. February 1, 1907. A portion of the tip of the middle finger is 
gangrenous; there is no infection; the distal phalanx seems to take part in the process of 
mortification. On the dorsum of the hand, just over one of the veins, there is a bean-sized 
indurated area; the skin over it is adherent and tender. About one inch above the wrist, 
behind the radius, there is a reddened hard cord, more than an inch in length (doubtless a 
thrombosed vein). 

The left foot is bluish, and there are a number of red nodosities in the leg. They are 
placed over the course of the long saphenous vein, one or two inches above the tip of the 
malleolus, and a couple of others three to four inches above the ankle. The right leg shows 
a thrombo-phlebitic, indurated process over the lower part of the anterior tibial group of 
muscles. 

Further Course .—The finger improves very slowly; in April it is healed. The nodules in 
the upper extremities disappear after three weeks. April 16, 1907, over the outer side of 
the right leg, four inches below the tibial tubercle, the skin and subcutaneous tissues are 
indurated. There are two hard areas farther down. The nodosities come and go, now in 
the right and now in the left leg. On April 29, 1907, his left foot troubles him greatly. 

It is slightly swollen; the toes become deep red in the dependent position. The right foot 
is slightly red in the same position. The femorals and popliteals pulsate well. On June 1 
the left foot is very painful; the toes feel as if needles were sticking them. 


288 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


November, 1907. Since the beginning of September the right leg seems to be affected 
by the same disease as the left. New nodules of subcutaneous infiltration have appeared 
on the inner side of the left leg and the inner side of the right knee. They seem to have very 
little tendency to disappear. He often has pain in the middle finger of the right hand, and 
this hand is colder than the left. 

Physical Examination. —On holding both hands above his head the right becomes 
blanched. When the hands hang, the right becomes cyanosed; there is an admixture of 
red, so that there is a mottling of red and blue (erythromelia of the upper extremity). 
Both radial pulses are good. Lower Extremities. —On the inner aspect of the right leg three 
nodules are seen, two near the tubercle of the tibia, a third one inch behind the middle of the 
crest of the tibia. They are H to i inch in diameter, involve skin and subcutaneous 
tissues, and are red. Similar infiltrations are found on the inner side of the left leg, two 
in the middle and upper third; two others four inches above the ankle. They evidently 
follow the course of the saphenous vein. The right foot has a bluish red color. The left 
is even more markedly discolored; the second toe is enlarged, looks angry, and presents a 
small superficial ulcer near the nail. On December 19 (a warm day) the legs are red when 
they hang down. There is no cyanosis. Both feet become cadaveric when raised. A new 
cord has formed over the right wrist; it is about an inch long, and lies over the radius; a 
somewhat longer cord is situated over the inner side of the right knee. (Mercury injections 
are administered.) January 3, 1908, the dorsalis pedis and posterior tibial arteries are 
pulseless. February 7 he still has the painful cord over the right wrist, although he has 
had seven injections of mercury. The right popliteal pulsates, the left pulsates faintly; 
both femorals are open. 

September 7, his right foot is worse than the left. The dorsalis pedis and posterior 
tibials of both legs are evidently closed. At this time the right popliteal does not pulsate; 
the left beats faintly (note that this corresponds with the aggravated subjective sensations 
of the leg); both femorals are felt. Recent ulceration has occurred in the web between big 
and second toes of the right foot. The toes are intensely red in the dependent position. 
On November 19, in the horizontal position both feet possess a marked erythematous hue. 

On April 13, 1909, the patient came to the hospital for the ulcerated condition of both 
feet; he cannot walk. Over the dorsum of both feet there are superficial ulcerations, and 
there are a number of trophic ulcers in the webs of several of the toes. Under rest in bed 
and local treatment all the wounds heal. By June 9 both legs are in a condition of chronic 
erythromelia, even in the horizontal position. The feet have a dusky red hue; in the 
dependent position there is an admixture of purple. The skin is shiny and appears thinned, 
although the toes themselves are enlarged. Only the femoral arteries pulsate; the ischemia 
in the elevated position is very marked; all the superficial ulcers have healed. 

Summary. —The total history up to the present time extends through a 
period of about twelve years. During the first eight years the clinical course 
was characterized by repeated attacks of migrating phlebitis of the superficial 
veins of the upper and lower extremities, and the appearance of cutaneous 
nodosities, due in all probability to circumscribed venous thromboses. These 
attacks were accompanied by the usual pain and tenderness, some edema and 
secondary cutaneous manifestations. Towards the end of the first period the 
prodromal indefinite pains of typical thrombo-angiitis were noticed. These 
were followed by the development of marked erythromelia of the left lower 
extremity, and of trophic disturbance. Then came a cessation of the process 
on that side, only to give way to a similar diseased condition on the right side, 
where it has caused obliteration of the distal vessels and the popliteal. In 
short, a period of occlusion of superficial veins was followed by a period of 
arterial occlusion which attacked first the left, and then the right leg. 

Does the paroxysmal nature of the involvement of the superficial veins 
throw any light on the sequence of events in the deep vessels? From previous 
pathological studies 1 it seemed most plausible to assume that certain territories 
of either arteries or veins become rather suddenly thrombosed , in a fashion 
similar to the superficial venous thromboses of the lower extremities. The 
history of the thirteenth case is exceedingly illuminating on this point, 
since it suggests that attacks of migrating phlebitis of one leg may occur 

1 Am. Jour. Med. Sci., October, 1908. 


TH ROM BO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 289 


synchronously with paroxysmal pains in the other leg, and that these latter 
pains are closely associated with other signs clearly pointing to an exacerba¬ 
tion of the thrombotic lesion in the deep vessels — 11 an attack (if we may so 
regard it) of thrombo-angiitis obliterans . ” In other words, it seems more 
than likely that, at any given time, the patient may be suffering from a more 
or less acute disturbance , in the course of which both superficial and deep vessels 
become closed. 

Case 13. M. P., 34 years, Russian Hebrew, admitted to Mt. Sinai Hospital in May> 
1908. My history was taken on May 24, 1908. Two years ago there were some “swollen 
places ” on both legs, and he had pain in the legs when he walked. One year ago he had 
attacks of “phlebitis;” this was the diagnosis at the Presbyterian Hospital. The veins on 
the inner side of the left forearm and arm, almost up to the armpit, were painful. The left 
saphenous at the middle of the leg was also diseased at that time. He had been treated at 
Mt. Sinai Hospital in August, 1907, for “phlebitis migrans.” At that time no suspicion 
was entertained as to the existence of the condition, thrombo-angiitis obliterans. 

Last winter he often had pain in the feet on walking, and this has been much worse for 
the past four weeks. During the last two months the symptoms of phlebitis have recurred 
in the left leg and the left arm. 

Present History .—For four days he has had excruciating pains in the calf of the right leg, 
even when in bed. Besides this, he has painful cords and “spots” in his left leg. 

Physical Examination. Both radials pulsate. The patient seems to be very restless 
because of the pain in his right leg. In the right leg neither the dorsalis pedis nor the pos¬ 
terior tibial artery can be felt; the popliteal artery is patent. The toes are slightly red in 
the horizontal position; there is marked erythema of the toes in the pendent position. 
Ulcers and thromboses are absent. (Note made May 24: The pain in this leg must be 
interpreted as suggesting thrombosis of the deep vessels, because there is nothing else to 
account for his suffering; apparently no neuritis.) 

In the left leg also, absence of pulsation in the dorsalis pedis artery and posterior tibial 
artery is noted. Just behind the tibia, at the middle of the leg, the saphenous vein is 
thrombosed, being adherent to the skin, which is reddened. There are a number of nodules 
in its vicinity, probably corresponding to small tributaries. There is erythromelia of 
moderate degree, but no marked ischemia in the elevated posture. The popliteal arterv 
is patent. 

In the left arm a small portion of an anterior ulnar vein, low down, is indurated. 

Briefly, then, the typical signs of bilateral thrombo-angiitis obliterans, without trophic 
disturbances, varicose veins, or infection, are associated with attacks of thrombo-phlebitis 
of the superficial veins of the upper and lower extremities. 

On May 28, 1908, the pain in the right leg is gone, the cords are disappearing, the ulnar 
thrombosis is no longer palpable. 

The patient again seen on December 1, 1908. After leaving the hospital he could walk 
but a block without stopping for a rest. For about two weeks a new longer cord has 
traveled up from the middle of the inner side of the left leg, behind the knee, to the lower 
part of the thigh. There is another one behind the ankle and inner side of the foot. In the 
calf there are two tender bean-sized nodosities. He says that the big toes always feel as if 
they were asleep, and he often has an inclination to rub them to dissipate the feeling of 
numbness. Examination shows his condition to be slightly worse than it was in May, 
as regards sufficiency of circulation in both legs. 

On June 15, 1909, he was again examined, then a pitiful spectacle to behold. 

Pulling himself along on two crutches, with an expression of fear written all over his face 
lest the contact of the soles of his feet against the ground call forth excruciating pain, with 
the aid of his wife he finally seats himself, telling me the following story: He has tried 
“everything” for his legs. He has been treated in other hospitals since I last saw him, and 
now he cannot walk at all. The big toe of the left foot hurts him unbearably, and his 
physicians are unable to ward off the coming of those dreadfully painful “sores” and 
‘fissures” that form without reason on his soles, between the toes, and near the borders of 
the nails. He cannot bear his weight on the legs at all. The effort to walk was soon given 
up and he has permanently assumed the horizontal position as the only one possible to be 
borne. 

Physical examination shows intense erythromelia of both feet, with a slight cyanotic hue, 
as in Case 12, D. B. The middle portion of the internal saphenous vein for about an inch 
of its course through the leg is converted into a hard, tender cord. There is a nodosity 
°-5 X 1 cm. three inches below the left tibial tubercle and two inches outside of the crest 
°tthe tibia. All the toes of both feet are somewhat enlarged; they look stiff and turgid 
when held in the dependent position. The blanching of the raised feet is extremfe. 

19 


290 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Resume of Case 13.—Recurring thrombo-phlebitis migrans of both upper 
and lower extremities, gradual development of the severe chronic clinical 
type of thrombo-angiitis obliterans without gangrene, symptoms indicating 
the simultaneous paroxysmal attack of superficial and deep vascular channels. 

One of the best examples of; extensive disease of the veins in all 
four extremities is that presented by Case 14. Because of the development 
of an adequate collateral circulation, obstruction and closure of the deep 
vessels had apparently produced no symptoms in the left leg, whilst the 
disease had made considerable progress in the right leg. Signs of an active 
migrating phlebitis could be found only in the lower extremities, but the 
definite statements of the patient leave no doubt as to the correctness of the 
view that he had had attacks of phlebitis in the upper extremities at one time. 

Case 14. M. G., 37 years, Russian Hebrew, married, has two healthy children, con¬ 
sulted me, August 6, 1909. Four years ago he had tender “cords” or “lumps” on both 
forearms and also on the inner side of the arms. These soon disappeared and have not 
recurred; at that time, however, there was also a similar condition in the calf of the right 
leg and inner side of the left leg. He was quite free from trouble until a year ago, when 
these painful spots also developed in the legs. 

For three months he has had wakeful nights because of pain in both feet, especially in 
the right. His toes get cold and he cannot walk because of the sudden advent of cramps in 
the calves. The “cords” in the right leg have now disappeared, but they are still present 
in the left leg, where they come and go. 

Physical examination, August 6, 1909. Both lower extremities present the typical 
signs of thrombo-angiitis obliterans. Evidences of circulatory insufficiency are most 
marked in the right leg, where there is distinct erythema in the horizontal and pendent 
positions. Both legs become intensely blanched when elevated. All three vessels (dor¬ 
salis pedis, posterior tibial, and popliteal) are pulseless on the right, whereas a very faint 
pulsation in the upper part of the left popliteal can be detected, the distal vessels evidently 
being closed. There are no ulcers. 

Just below the middle of the course of the left saphenous a hard, knobbed, tender cord 
can be easily felt. At the inner border of the foot there is an erythematous nodule which 
is tender. 

On August 8, about 1 inch of the thrombosed saphenous of the left leg was excised 
under local anesthesia for diagnostic purposes. The vein was filled with recent clot, and 
was fairly adherent to its bed, showing an active periphlebitis. 

In September, 1909, the right leg was amputated three inches below the knee, because 
of gangrene of the toes. 

On October 27, 1910, he says that there was considerable pain in the sole of the left foot, 
and that he could not walk more than two blocks without stopping for rest. Ever since the 
operation he has had recurrent attacks during which the same hard cords or nodules which 
he had before, developed in the left leg. Several of these have now been present for three 
weeks. 

Physical examination, October 27, 1910, shows a nodosity in the middle of the left leg, 
and two or three confluent nodosities above the malleolus. There is marked erythromelia, 
and the pulses are absent in the popliteal, posterior tibial, and dorsalis pedis. 

November 10, 1911. The phlebitic process is still present. Fresh nodules are making 
their appearance. The evidences of obliteration of deep vessels of the left leg are more 
striking, and the disease, thrombo-angiitis obliterans, is evidently making progress with 
signs of the development of trophic disorders. 

Epicrisis. We are dealing here with a case of bilateral thrombo-angiitis obliterans with 
associated migrating phlebitis which had originally affected both forearms, and for more 
than two years has shown itself also in the lower extremity. The persistence of the migrat¬ 
ing phlebitis, the chronicity of the deep vessels, and thrombo-angiitis obliterans of the left 
leg, are features worthy of note. 

Here we are dealing with a case presenting active signs of thrombo-angiitis of the vessels 
of the lower extremities for three months. At the same time, there were recurring attacks of 
phlebitis of the upper and lower extremities. At times he sought advice because of the 
phlebitis; at other times, because of the symptoms referable to the deep seated disease. 
Four years after the onset of the disease the findings were as follows: 

The results of advanced closure of the arteries of both lower extremities; absence of any 
recent or active symptoms in one of the legs; distinct signs of a slowly progressing involve¬ 
ment of the circulation of the other limb, with recurring attacks of phlebitis of the saphe¬ 
nous vein, without ulcers, trophic disturbances, varicosities, or evidences of inflammation. 


TH ROM BO-A NGIITIS OBLITERANS—MIGRATING PHLEBITIS 291 


VI. EXTENSIVE FULMINATING MIGRATING PHLEBITIS 

By this type we mean cases in which from the very first onset of the 
thrombo-phlebitic process, there is not a single period of remission but attacks 
of migrating phlebitis follow in quick succession one after the other, so that 
the whole of the foot and the greater part of the leg and even the thigh are 
beset with the inflamed and indurated cords. That the process is a severe 
one and may have analogy in the deep veins was demonstrated by the clinical 
course and pathological findings in one of the cases (H. H.) in which at the 
time of amputation the popliteal vein was found in a condition of diffuse 
phlebitis and obturation with red clot, the femoral vein found to be likewise 
involved at a secondary operation. 

Case 15. H. H., Russian, 36 years of age, consulted me on the 15th of April, 1916, with 
all the usual symptoms of thrombo-angiitis obliterans of both lower extremities, with absent 
dorsalis pedis, posterior tibial and popliteal pulsation on both sides, without migrating 
phlebitis. 

From August 20, 1919 (probably several months before this, according to the history), 
until amputation was done on the 15th of March, 1921, a period of about two years, there 
had been a succession of attacks of migrating phlebitis, particularly over the left leg and 
thigh, which were exceedingly painful, and caused the patient to stay most of this time in 
bed. 

On the 20th of August, 1919, there were evidences of thrombo-phlebitis over the internal 
saphenous of the left leg, that had, according to the history, been present for several months. 
On the 4th of November, 1919, the phlebitis had somewhat subsided, having lasted now 
about one-half year. In December, 1919, another attack of phlebitis took place. 

On April 2, 1920, he said that for the last three months there had been constant attacks of 
migrating phlebitis with tender and red areas, making it impossible for him to work, and 
the right hand as well as both feet are cold at all times. Throughout the rest of the year 
attacks followed in quick succession so that the greater part of all the superficial veins 
were involved. 

The pain in this case (as well as in others of this type) was excruciating by 
reason of the multiplicity of veins involved, and with this the limb seems to 
become daily more and more atrophic. 

Finally, on the 15th of March, 1921, a Gritti-Stokes operation was performed, and not 
only was the popliteal artery closed by old organized clot, but the popliteal vein was occu¬ 
pied by a recent clot similar to that found in the superficial veins. 

Contrary to the rule, this case did not do well after the Gritti-Stokes operation (being 
the only case in a series of more than sixty), since the peripheral portions of the flaps became 
gangrenous, the sloughing process continuing in spite of rigid asepsis and great care. 

It became necessary, therefore, on the 26th of April, 1921, to do an amputation through 
the thigh, where an explanation for the inadequate circulation was to be found in the 
condition of a femoral vein, which was also closed by red thrombus. 

Summary .—Extensive migrating phlebitis of two years’ duration, with practically no 
remissions, a thrombotic process involving the femoral and popliteal veins, interfering with 
circulation to such an extent as to prevent healing, when Gritti amputation was done. 


VII. CASES IN WHICH ABSOLUTE EVIDENCES OF DEEP ARTERIAL 
INVOLVEMENT ARE LACKING 

Although our experience justifies the conclusion that the affection of the 
deep arteries or veins regularly follows the premonitory migrating phlebitis, 
even though years elapse, occasionally cases are observed in which evidence 
of arterial involvement is absent for so long a time that we are in some doubt 
as to the correctness of our diagnosis. Eventually at least one or more pulses 
become imperceptible even though local symptoms are lacking. 

We may summarize briefly the history of one instance, in which the attacks 
of thrombo-phlebitis must have been distributed over a period of 8 years, 


292 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


during which time signs of blockage in the deep vessels were not demonstrable. 
Finally, io years after the first attack of phlebitis, the posterior tibial pulses 
could not be felt. 

Case 16. B. S., male, Russian, aged 36, gives a history of swelling and reddening of both 
legs of 8 years’ duration, accompanied by “hardening” of the veins and inability to walk. 
Similar disturbances have been intermittently present in both upper extremities for the 
last 2 years. 

Physical examination, August 23, 1920, none of the subjective or objective manifesta¬ 
tions of thrombo-angiitis obliterans could be elicited in the lower extremities. There was a 
long cord over the ulnar half of the anticubital aspect of the forearm, and several tributaries 
of the external and internal saphenous of the right leg were the site of migrating phlebitis. 
A small vein of the right forearm was also involved. All the arteries of the lower extremi¬ 
ties pulsate at the usual sites. 

August 24,1920, excision of a tributary of the left ulnar vein for microscopic examination 
revealed an occluded vein with thickened walls, and adherent to the skin, and its lumen 
filled with clot in very early state of organization. Microscopic examination revealed 
the typical picture of thrombo-angiitis obliterans in the acute stage. 

December 1, 1922. There have been no symptoms since August, 1920; no intermittent 
claudication, no manifestations of impaired circulation of the lower extremities, and no 
recurrence of the phlebitis. Nevertheless, examination shows that both posterior tibial 
pulsations have disappeared! 

These facts lead us to the following conclusions: 

First, that the phlebitis plays no subsidiary role in the symptom-complex 
of some of these cases. 

Second, that the disease, when it affects the upper extremities, is less endur¬ 
ing than in the lower extremities. 

Third, that we have here another link in the chain of evidence speaking 
for an identical cause for the disease of the deep arteries and veins and the 
superficial veins. 


CONCLUSIONS FROM VEIN LESIONS 

In 1908 the author’s studies of the pathology of nineteen amputated limbs 
in thrombo-angiitis obliterans had clearly demonstrated the thrombotic 
nature of the vascular occlusion. It was also shown that the pictures formerly 
interpreted as results of a thickening of the inr'ma were produced by 
organization and canalization of red obturating thrombi. It was found that 
the disease involves the deep arteries and veins of both the lower and upper 
extremities, commencing by preference in the vessels of the foot, such as the 
dorsalis pedis and plantars and their larger branches, ascending so as to 
sometimes close even the iliacs and aorta. Clinical and pathological data led 
to the assumption that the progression of the thrombotic process takes place rather 
in' attacks or sudden exacerbations than by a gradual ascent; that larger or 
smaller territories of the deep vessels become suddenly closed, just as the 
saphenous veins are wont to be thrombosed and inflamed from other causes— 
in other words, that the process is a migrating thrombosis of the deep vessels 
comparable to the migrating phelbitis of the extremities. 

A cursory study would lead one astray as to the significance of the most 
common lesions seen in the arteries and veins, for it would fail to reveal the 
fact that there are two distinct phases in the pathology of the disease. The 
lesion most commonly encountered is but the result of the organization of 
thrombi, and of importance only in so far as it is productive of the pictures 
that may be confused with endarteritis obliterans. More interesting and 
more valuable for investigation is the “acute stage,” or earliest lesion, that 
occurs simultaneously with, or shortly after the onset of the thrombosis. 


TH ROM BO-ANGIITIS OBLITERANS—MIGRATING PHLEBITIS 293 


This early stage was found by the author in the deep vessels of but two of the 
amputated limbs. In these certain specific morphological alterations were 
encountered, whose meaning was not understood at that time. These histo¬ 
logical changes appeared to be characteristic of the disease, thrombo-angiitis 
obliterans, not having been met with in vessels thrombosed through other 
causes. The regularity of the occurrence of the typical lesions aroused the 
suspicion that here was a specific morphological alteration, due to a specific 
cause. 

In short, whereas the usual changes in most of the vessels of an amputated 
limb represent the healed stage of the disease, that in which a fibrous mass 
containing canalizing vessels has taken the place of the original clot, there is 
another early or acute stage of the disease which alone is of value in throwing 
light upon the true nature of the process. It is only at this particular period 
in the history of the pathological process that the media is diffusely infiltrated 
with leukocytes, and that the lumen is filled with red clot, in which certain 
typical miliary giant-cell foci 1 make their appearance. It is these foci that 
lend a characteristic appearance to the thrombotic lesion of thrombo-angiitis 
obliterans. 

When these lesions were first referred to in 1908 their significance was 
not understood, although the suspicion was already aroused at that time 
that they were specific for the disease and probably represented a peculiar 
reaction on the part of the tissues to some toxin or organism. It seemed clear, 
too, that it would be a difficult matter to obtain an adequate amount of mate¬ 
rial from the deep vessels for the study of the acute stage of the disease. It was 
here that we had to pause in our deductions, when we were fortunate enough 
to encounter a most interesting fact, that the superficial or subcutaneous 
veins of the upper and lower extremities may also be affected by the disease, 
thrombo-angiitis obliterans. Thus, in 1909, the association of migrating 
phlebitis of the subcutaneous veins of the extremities was noted in eleven 
cases. From a study of the clinical history of the cases, and of the histology 
of the affected subcutaneous veins exsected during various stages of the 
disease, the following conclusions were drawn: 

1. The disease thrombo-angiitis obliterans is often associated with 
thrombo-phlebitis of superficial veins of the arms and legs. 

2. Certain peculiar cutaneous nodosities are characteristic manifesta¬ 
tions in many cases. 

3. The disease of the superficial veins may be subsidiary or it may 
dominate the clinical picture. Objective signs referable to these vessels 
should be regarded as extremely suspicious marks of the synchronous develop¬ 
ment of thrombo-angiitis obliterans, in the form of pulseless vessels, erythro- 
melia, blanching of the leg in elevated posture, cold and blue toes, pain in the 
calf of the leg brought on by walking, and other typical phenomena. 

4. Migrating thrombo-phlebitis may give no symptoms, the signs refer¬ 
able to the deep vessels being of most importance. 

5. Patients may suffer at one time from migrating thrombo-phlebitis, 
at another from the progress of the occlusive change in the deeper 
vessels. 

6. Certain cases suggest the possibility that attacks of trouble in surface 
veins may occur simultaneously with similar exacerbations of disease in 
deep vessels of another limb. 

1 Buerger, Mitteilungen aus den Grenzgebieten der Medizin und Chirurgie, 21 Band, 
1919; also Am. Jour. Med. Sci., October, 1908; and Surg., Gyn. & Obst., Nov., 1914. 


294 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


7. The morbid process resulting in the production of cutaneous nodosities 
and thrombosed superficial veins is independent of varicosities, of infection, 
or of trophic disorders in the territory which they drain. 

8. The vessels of the upper extremity may be affected by the lesion 
thrombo-angiitis obliterans. 

9. Thrombo-phlebitis in the arm and forearm should arouse suspicion 
as regards involvement of the deep vessels of the legs. 

10. Further studies should be directed towards solving the relationship 
between the two thrombotic lesions. Perhaps excision of nodules and veins 
early in the disease, exploratory incision for inquiry into the condition of the 
deep vessels, and bacteriological and serum investigations along the proper 
lines will do much to enlighten us in our interpretation of this most puzzling 
symptom-complex. Although absolute proof is lacking, it seems more than 
probable that the same determining causative factor is responsible for the 
lesions of both the superficial and deep vessels. 

Up to the year 1922 it was possible to gather data on additional cases in 
which the superficial veins were involved which increased the number of 
exsected veins up to thirty-five. In these, both the acute and healed stages 
of the disease were found. From a consideration of the pathological pictures 
the conclusion was reached that the specific characteristic lesion of thrombo¬ 
angiitis obliterans may affect the deep as well as the superficial vessels;, that it 
is in the veins that we shall have to look to find material for investigation of 
the causative agent; and that not only do the superficial veins present the 
typical miliary giant-cell foci, but they also demonstrate that these foci are 
a later stage, or attempt at organization of purulent foci. In other words, 
the finding of miliary pus foci in the subcutaneous veins as precursors of the 
typical giant-cell foci was noted in a sufficient number of instances to warrant 
the conclusion that this lesion represents the acute stage of the disease, and 
suggested, too, that the thrombotic process may be caused by the presence of 
some organism, virus, or specific toxin. 


CHAPTER LIX 

THROMBO-ANGIITIS OBLITERANS—INVOLVEMENT OF THE 
UPPER EXTREMITIES 

In about 500 cases of thrombo-angiitis obliterans observed from 1909 
to 1922, the author was able to watch the course of this remarkable disease 
through all its clinical stages. Many of the cases were followed from 
five to fourteen years, and the presence of interesting mutations in the 
symptomatology could be recorded. It was found that in a certain number 
of the patients the upper extremities are involved, although it is usually 
believed that only the lower extremities are affected. 

Early Symptoms of Involvement of the Upper Extremities. —Coldness and 
a feeling of numbness and deadness of the fingers may be the first symptoms 
in one or both hands simultaneously, trophic disturbances soon following. 
Patients describe these as being sores at the tips of the fingers that are exceed¬ 
ingly painful, that are sometimes followed by suppuration gradually healing, 
leaving retracted scars near the nail at the tips of the affected fingers. Pallor 



THROMBO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 295 


of one or more fingers in cold weather is also mentioned by patients as a 
striking symptom. 

Objectively, when seen several months after the onset of the symptoms, 
the picture of early involvement without gangrene and without trophic lesions 
is the following. The hands may show rubor and this is associated with cold¬ 
ness of the tips of the fingers. This combination of diminution of 
temperature with the usual objective manifestations of heat is paradoxical 
but characteristic of thrombo-angiitis obliterans. The tips of the fingers 
may be slightly cyanotic or a cyanotic hue over the proximal portion of the 
nail bed is present. 

The retracted sores at the tips of the fingers are apt to lie in whitened 
thinned-out skin, and although completely healed, are exceedingly sensitive 
to the touch. 

With these manifestations the radial pulse may be absent in one or both 
hands. The circulatory manifestations do not bear the same relationship to 
posture as in the lower extremities, for ischemia may be absent on elevation, 
or if present, may be very slight. 

In some cases the incipiency of this affection in either the ulnar or radial 
arteries manifests itself in the coldness of one or more fingers only, and on 
examination one of these two arteries may be closed, one or two fingers 
distinctly cold, with a tendency to pallor. If an Esmarch be applied to the 
arm, the differences in circulation between the affected fingers and the others 
can be made more evident, for the reactionary hyperemia will be sluggish 
in appearing in the territory of impaired circulation. 

A surveytof many histories shows that the upper extremities may be 
clinically involved in the following ways: (I) without subjective symptoms; 
(II) with vasomotor symptoms predominating; (III) with lesions simulating 
the results of neurogenic disturbances; (IV) with trophic disturbances alone; 
(V) with trophic and vasomotor phenomena; (VI) with gangrene of slight 
extent; (VII) with extensive gangrene threatening the viability of the 
extremity; (VIII) with extensive atrophy of the hand and forearm; (IX) 
with changes simulating scleroderma and sclerodactyly; and (X) cases with 
acute arteritis of portions of the radial or ulnar artery (migrating arteritis). 

I. Thrombo-angiitis Obliterans of the Upper Extremities without 
Symptoms.—Just as in thrombo-angiitis of the lower extremities, there are 
cases in which the radial or ulnar artery, or both, become gradually closed 
without the patient’s experiencing any noticeable symptoms. In some 
instances, absence of pulsation was discovered during a routine physical 
examination; in others, where symptoms were present in the lower extremities 
investigation of the radial and ulnar vessels had demonstrated their occlusion. 

J. A., male, aged forty years, Russian, began to have trouble in the right leg ten years 
ago (1904), pain coming on during walking, subsiding when at rest. Gangrene of the little 
and of the big toes developed, leading to amputation of the left leg at its middle in 1906. 
Since 1908, similar symptoms involved the left leg, and the first and second toes became 
ulcerated, also requiring amputation. During the period of clinical observation the right 
radial pulse gradually disappeared, although no vasomotor or trophic manifestations could 
be elicited on examination. The patient was lost sight of so that the further course could 
not be followed. 

The symptoms of Raynaud’s disease, too, may be closely mimicked, as 
in the following cases: 

II. Cases in Which Vasomotor Phenomena Preponderate.—Such an 
instance is described in the following history, where, after about ten years of 
migrating phlebitis, and the usual circulatory disturbances of the lower 


296 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


extremities, distinct evidences of involvement of the vessels of the arm and 
hand supervened. 

The following history denotes an instance of remarkably striking vaso¬ 
motor manifestations that are either part of the thrombo-angiitis obliterans 
syndrome or coincident with it. When we are confronted with neurotic 
manifestations suggestive of chronic acroasphyxia as here, a long period of 
clinical observation may be required in order to determine accurately whether 
two types of vascular disorder, neurogenic and organic obstructive are not 
simultaneously represented. Certain it is that vasomotor phenomena may 
accompany thrombo-angiitis obliterans as a part of the latter’s symptom- 
complex. 

J. V., male, aged thirty-four years, Russian, admitted to the hospital December 17, 
1907, says that three and a half years previously he noticed that his fingers were cold 
but not blue. The following winter the same symptoms returned, but, in addition, the 
skin of the tip of the right middle finger became dry and a “wound” spontaneously 
developed. For the past two years his hands would get blue, cold, and numb on exposure 
to cold, their natural color returning in a warm room. There was never any pallor. A 
sort of “sticking” pain in the finger tips would regularly accompany the state of blueness. 

Physical examination , December 17, 1907. Both hands are deeply cyanotic up to the 
wrist, and very cold. During the examination bright red or crimson colored spots can be 
seen to appear in the dorsum and palm. Over the back of the hand these red blotches 
become very distinct and do not shade off into the blue areas. The two distal phalanges 
remain deep blue. If the hands be observed for a still longer time (five minutes) the red 
color becomes paler and is mottled with a yellowish pink; at times a totally different and 
much lighter shade, variegated with red and blue, will completely replace the deep colors 
first noted. In the palm the red areas are not so apparent, but they also give way at times 
to. the lighter shades. The terminal phalanges of the ring fingers are enlarged, those of the 
middle fingers somewhat less so. When the hands are held above the head for two or more 
minutes the redness disappears, a pale sickly purple remaining. The radials and brachials 
pulsate well. 

In the lower extremity a similar picture is present, but there are evidences of obliteration 
of the vessels. The right dorsalis pedis cannot be felt, although palpated on many occasions 
from December 17, 1907, to January 20, 1908. In the left dorsalis pedis there is fair pulsa¬ 
tion. There is ischemia in the elevated position of the legs, as evidence of the impaired 
vascular supply, and bespeaking the presence of the lesion, thrombo-angiitis. 

If such an exquisite example of vasomotor disturbance can belong to a 
case of thrombo-angiitis obliterans, there is little wonder that confusion should 
exist in the differentiation of the symptoms due to neurogenic and organic 
vascular affections. 

A. B., male, aged thirty-one years, Russian, noticed the appearance of small hard lumps 
under and in the skin of the calf of both legs in 1904 (ten years ago). They were painful, 
lasted for a few days or a week or more, and would then disappear (migrating phlebitis). 
For three years similar lumps and strands would come and go over the lower and inner side 
of the right thigh. About seven years ago he began to experience cramp-like pain in the 
right foot and calf of the leg on walking. Later the right foot became “cold.” An ulcer 
developed on the third toe and showed no tendency to heal. 

For seven years he has been suffering with similar symptoms in both legs and feet, the 
typical symptoms of pulseless vessels, erythromelia, ischemia in the elevated position, and 
gangrene of several toes being present. He now (1914) has already lost four toes of the left 
foot and two of the right. 

Four months ago his right hand began to trouble him. In cold weather it would become 
very pale, particularly the little finger. On warming the hand, color would gradually 
return. Of late, however, the tip of the little finger has been bluish for days at a time, 
although excessive heat seems to bring back a normal color. 

Physical examination, May 6, 1914. The radial and ulnar arteries of both sides pulsate 
distinctly. Both hands, perspire profusely, and are somewhat cold. The tip of the little 
finger of the right hand is cyanotic and deeply discolored over its palmar aspect. Pressure 
over this part elicits some pain. Roentgen-ray examination of the hand is negative. 


THROMBO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 297 

On July 31 , 1914, patient says that the little finger and thumb of the right hand feel cold. 
Scales form on the tip of the little finger, and when these separate, leave a healed depression. 
He has no pain. 

Physical examination shows that both the little finger and the thumb are distinctly cold 
to the touch, the coldness extending to the base of the fingers. The other hand and fingers 
are warm. The radial and ulnar arteries pulsate well. On elevation there is no appre¬ 
ciable change in the color of the fingers. 

In short we have an example of thrombo-angiitis in which vasomotor 
symptoms initiate the onset of the disease in the upper extremities. Previous 
experience warrants the assumption that we may either expect a complete 
cessation of the symptoms in the hands, if adequate collaterals be established, 
or progressive occlusion of vessels until the radial and ulnar arteries become 
obliterated or until gangrene ensues. 

III. Cases with Lesions Simulating Neurogenic Disturbances.—The 

following picture was characteristic in certain of the cases in which thrombo- 



Fig. 49. Atrophic and dystrophic changes in the fingers and nails in thrombo-angiitis 

obliterans. 


angiitis obliterans of the lower extremities had already been present for a 
long time, necessitating amputation of one of the lower extremities. 

All the fingers of the affected hand are tumefied and have an exaggerated 
conical appearance due to relative abnormal increase of the girth of the prox¬ 
imal portion of the fingers. The general swelling is such as to obliterate all 
of the normal furrows and markings. The texture and color of the skin also 
are altered in that portions of the skin, particularly about the nails, have a 
glossy appearance. The integument (Fig. 49) appears stretched over swollen 
subcutaneous tissues, and the color, too, is peculiar in that there is a diffuse 
reddening of the distal digits. There seems to be a subungual trophic distur¬ 
bance manifesting itself by discoloration of the nails. As a result, the lunula is 



298 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


increased in size to four or five times the normal. One or more of the fingers 
may show the absence of the distal portion of the last phalanx, and depressed 
scars, at the bottom of which a necrotic section of the bone may protrude. 

The palmar aspect of the hand and fingers shows a general tumefaction 
and reddening. Both the radial and ulnar arteries usually fail to pulsate. 

In addition to the objective manifestations, there may be limitation of 
motion in most of the phalanges. 

In the case described below, the employment of hot baths, intermittent 
compression of the brachial artery was followed by rapid diminution of the 
edema and intensity of the rubor, and by improvement in the temperature of 
the fingers. 

In rare cases there are atrophic changes in the bones of the hand associ¬ 
ated with articular changes that do not show any evidence in the X-ray, but 
lead to ankylosis. The bone lesions differ from sclerodactyly in that there is 
no change in the terminal phalanges even though defects in the soft parts may 
occur. The most marked lesions in the bones are absorption and rarefica- 
tion of the radius and ulna and carpal bones, of the bases of the metacarpal 
bones, and of some of the phalanges. 

The history in one of the typical cases was as follows: 

R. L. was observed from July 23, 1912, till March, 1921. In January, 1912, he was 
twenty-nine years of age, with the usual symptoms of thrombo-angiitis obliterans of the left 
lower extremity, with the typical erythromelia, and absence of dorsalis pedis and posterior 
tibial pulsation. The process was progressive; on the 8th of March, 1918, it had advanced 
so as to involve both extremities. There had been ulcerations of the toes of both feet. 
The right leg was amputated in 1918. March 17, 1912 he consulted me because 
of severe pain in the right hand radiating to the wrist, and because of the discoloration of the 
nails and of the fingers. He says that the first sign of trouble in the right hand, was the 
absence of the radial pulse, which he felt repeatedly, having a good knowledge of the signi¬ 
ficance of pulsation, and fearing that the right hand might be involved. About eight 
months ago, spontaneous gangrene of the tip of the ring finger of the right hand occurred, 
and following this the other fingers became swollen and reddened. 

May 5, 1921, rubor still present, but rather diminished. The opaque portion of the nail 
is greater than before. 

The disappearance of such marked symptoms 18 months later is worthy of note; 
Oct. 26, 1922, remarkable improvement in the condition of the right hand, the chronic 
rubor having disappeared. The fingers have taken on a more healthy appearance, the only 
evidences of disturbance being the retracted scar at the tip of the ring finger of the right 
hand where a piece of bone had separated; and the somewhat atrophic condition of the skin. 
The right brachial artery can be felt beating in its upper part, but its pulse is imperceptible 
below the middle of the arm, although it is easily palpated. The left brachial artery can be 
felt all the way down. Just as remarkable as the disappearance of the chronic erythromelia 
and the normality of the nails and nail-beds, is th e freedom of motion in the interphalangeal- 
joints, in which the fixation 18 months previously seemed sufficiently advanced to threaten 
chronic ankylosis of the joints. 

This pseudo-ankylosis appears at first sight to be due to joint involvement. 
However, it was observed to disappear in the following case, as the vaso¬ 
motor and trophic disturbances gradually improved. Perhaps the fixation 
is of the nature of those sympathetic contractures that the French authors 
attribute to derangements of the periarterial sympathetic. The extensive 
obliteration of the radial and brachial arteries with the periarteritis that 
accompanies would seem to substantiate such a theory, although such con¬ 
tractures and fixations are but rarely observed. 1 

Another striking instance of the association of vasomotor symptoms and 
trophic lesions is the following: 


1 See Chaps. LXXXVI, XCI, and CV. 


T H ROM BO-A NGIITIS OBLITERANS—UPPER EXTREMITIES 


299 


A. W., 24 years, a Russian Hebrew, had thrombo-angiitis obliterans of both legs 
necessitating amputation of the right leg. 

November 8, 1922. For some weeks there has been pain in the fingers of the right hand 
coldness, varying discoloration of the fingers, and an ulcer developed at the tip of the ring 
finger. 

Physical Examination. The right hand has a peculiar variegated appearance due to the 
difference of color in the various parts of the fingers, and the abnormal appearance of the 
nails of the second, third and fourth digits. 

Color changes take place while under observation, in that parts of the fingers are deeply 
cyanotic, and other parts have a more scarlet hue; still other areas have a yellowish ashen 
tint. Over the tip of the fourth finger, near the nail-bed, there is necrosis of the skin and 
an accumulation of fluid under the adjacent skin, the whole region being deeply cyanotic. 
All the fingers are slightly swollen. 

The radial and ulnar arteries do not pulsate, but the brachial artery can be felt down to 
the elbow. The pulses of the left hand are normal. 

The texture of the nails is entirely changed, being completely whitened and having the 
appearance of celluloid or sea shell, this due to an opacity that does not permit the matrix 
to shine through. They seem abnormally convex and prominent. 

IV. Cases with Trophic Disorders Only— In some patients, distinctive 
signs of an affection of the upper extremities manifest themselves as trophic 
disturbances not extensive enough to lead to gangrene. The disease may be 
wholly overlooked by the patient and, when the lesion has healed, it may be 
subsequently referred to by him as a slight “sore” or “ulcer” developing 
without cause. Were it not for the presence of the disease in the lower 
extremities and for the changes in the radial pulse the nature of the trophic 
disorders would be difficult of solution. 


T. S., aged thirty-one years, Russian, consulted me in May, 1914, because of the 
condition of his left foot. Three and a half years previously he experienced pain in the sole 
of the left foot on walking and was treated for rheumatism. Two years after the onset a sore 
developed between the fourth and fifth toes of the left foot and another one on the tip of the 
big toe of this foot. Since then the foot became red and the little toe gangrenous, falling 
off about a year ago. About this time his right leg began to trouble him, the symptoms 
being pain in the calf on walking. 

Two and a half months ago there developed a spontaneous ulcer over the middle 
phalanx of the right hand, not accompanied by any evidence of inflammation, hardly pain¬ 
ful, and not brought about by any injury. He was treated for this for about eight weeks, 
when the wound healed. 

Physical examination, May, 1914. Over the middle phalanx of the right hand there is 
an irregularly shaped scar, about 8 mm. in length and 4 mm. in width, evidently the site of 
the old healed lesion. The right radial pulse is not perceptible. 

We have here a typical case of thrombo-angiitis of the lower extremities, 
first involving the left then the right lower, extremity, and three years later 
manifesting itself also in the hand, with trophic disturbances and oblitera¬ 
tion of the radial artery. 

V. Cases with Trophic and Vasomotor Phenomena. —It is rather charac¬ 
teristic of the symptomatology of the disease as it affects the upper extremi¬ 
ties that manifestations are frequently overlooked by the patient, until 
definite objective signs, such as trophic ulcers, make their appearance. The 
almost inexplicable development of such phenomena may lead to careful 
examination on the part of the physician, and to the detection of the absence 
of the radial or ulnar pulse, or even the brachial. The chronological 
sequence of events in a number of these cases is the following: 

(1) Symptoms of thrombo-angiitis obliterans of the lower extremities, 
with or without amputation of one extremity, or ulcers of both, over a period. 

(2) A stage of involvement of the upper extremities with ulcers, and 
disappearance of the pulses in this territory. 


300 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


(3) A chronic period with more or less permanency of symptoms both 
in the lower and upper extremities, a condition of vasomotor lability and 
impaired circulation of the hand being a striking development. 

S. S. S., 37 years, born in Russia, consulted me on the 19th of September, 1922, with a 
history of having had an amputation of the left leg, and complaining now of pain in the right 
foot; inability to walk, ulcers of the big and little toes, coldness, discoloration of the foot; 
also of numbness of the tips of the fingers of both hands, and a chronic fissure or ulcer on 
the middle finger of the right hand. 

Six years ago he began to experience pain in the left foot, and phlebitis was recognized. 
In 1918 a diagnosis of occlusion of the blood vessels of the left leg was made. After the 
removal of a callous a wound developed, which did not heal, and the foot became progress¬ 
ively worse. He was treated until September, 1920, when amputation of the left leg had 
to be performed. 

In October, 1921, the right foot began to annoy him, and shortly thereafter ulcers 
developed over the big and little toes of the right foot. In January, 1922, the big toe 
became bluish and the wound was still not healed. Then improvement occurred, but 
another ulcer developed 3 weeks ago on another toe, and the foot became very painful. 

The History of the Upper Extremities .—As far as he knows there were no symptoms 
referable to the upper extremities until January, 1922, when ulcers developed at the tips of 
the second and third fingers of the left hand. Since then, however, both hands became 
numb and cold , and bluish discoloration has been regularly noted in cold weather; latterly 
even at room temperature. Within the last 2 weeks he complained of numbness of the 
right hand. However, as far back as January, 1922, he was told that the ulnar and radial 
pulses of both hands were not palpable. 

In short, an old history of thrombo-angiitis obliterans of both lower extremities followed 
by the development of ulcers on the tips of the second and third fingers, closure of both 
ulnars and radials having already been present, when the ulcers appeared. 

Physical Examination. —On the left there is a stump, amputation having been performed 
above the knee. The right leg is in a condition of intense erythromelia, both the dorsalis 
pedis, posterior tibial and popliteal pulses being absent. The right and left femorals pul¬ 
sate. The coldness of the foot extends up almost to the ankle. 

The Upper Extremities. —The tips of all the fingers are markedly cyanotic, particularly 
those of the left. The lividity extends almost to the bases of the first phalanges over the 
volar aspect of the left hand, and not quite so far centrally on the dorsal aspect. The 
cyanosis is less marked on the right. The fingers are cold, as far as 1 inch beyond the meta¬ 
carpal phalangeal joints on the left, and up to the metacarpal phalangeal joints of the right 
hand. Both ulnars, both radial, and the right brachial arteries do not pulsate. The left 
brachial pulse is small. 

On elevation of the hands there is a moderate degree of blanching, but the cyanosis is 
exaggerated in this position. The tips of the index and middle fingers of the right hand 
show cicatrices and retracted fissures near the nails. Similar, but less marked lesions are 
present in the same situation in the left hand. Both hands show marked reactionary 
rubor after preliminary elevation, especially the right hand. 

Comments .—It is rather noteworthy that in spite of the extensive obliterac 
tion of the arteries of the upper extremities here, such minimal trophi- 
disturbances should have developed. As contrasted with the appearances 
of the lower extremities in such cases, and as well illustrated in this case, the 
intense cyanosis may characterize the upper extremities, whilst a marked 
degree of rubor is present in the foot or feet. That vasomotor phenomena 
play a role in producing the exaggerated lividity, seems evident, for 
variations in the degree of asphyxia frequently occur, and much of it may 
disappear and give way to reactionary erythromelia when the arms are 
elevated and depressed secondarily for a number of times. Whether a 
venous spasm plays a role is worthy of investigation. The intensive 
asphyxia of the hands in some of these cases might lead to the tentative 
diagnosis of chronic acroasphyxia, if careful attention is not given to 
palpation of the pulses. 

VI. Cases with Gangrene of Slight Extent.—Not a small number of the 
patients that suffer with occlusion of the vessels of the upper extremities 
come to us with a history of having had pain in the tip of one of the fingers 


THROMBO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 


301 


for a considerable time. This is followed by a change in the color of the skin, 
usually reddening of the tips of the fingers, as if they were inflamed. Later 
there develops a sore or the skin changes color and becomes gangrenous, 
usually at the tip of a finger, although the lateral margin of the finger may 
be first affected. 

M. S., aged forty-seven years, Russian, was admitted on June 25,1907, giving the follow¬ 
ing history: About eight or nine months ago he noticed that the fourth toe of the left foot 
was cold, blue, and painful. About four months ago the pain became so severe that he 
consulted a physician, who told him that an infection had taken place. Since this time a 
sore developed under the nail and the nail-bed became black. 



Fig. 50.—Gangrene of the tip of the index finger. 


Physical examination showed complete gangrene of the distal half of the fourth toe of the 
left foot, absence of pulsation in the dorsalis pedis artery, an area of superficial gangrene of 
the skin on the dorsum of the foot, intense erythromelia (hyperemia of the foot) in the 
dependent position, and marked ischemia in the elevated position. June 28, 1907, amputa¬ 
tion was done through the tarsometatarsal articulation. On July 5, re-amputation was 
done through the middle third of the leg, the wound healing slowly. 

In 1910 the disease began to involve the right leg in the same typical manner, leading 
also to dry gangrene of the fourth toe. When examined in March the popliteal, posterior 
tibial, and dorsalis pedis of the right leg could not be felt. 

In short we have a typical case of thrombo-angiitis obliterans, first involving the left 
lower extremity leading to gangrene, amputation, and some three years later involving the 
right leg. 

In March, 1914, I again saw the patient, who now complains of symptoms in the left 
hand. 

March 18, 1914. For several months he has had pain in the tip of the left index finger 
and lately the finger has changed color becoming withered and glossy. 

Physical examination shows an ulcer at the tip of the left index finger, the live skin above 
it atrophied and glossy, the hand somewhat smaller than the other, and the fourth finger of 
the same hand distinctly shrunken. The radial pulse of this hand cannot be felt (Fig. 50). 



302 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

We are evidently dealing here with a case in which some seven years after 
the onset of the disease in the lower extremities, the left upper extremity 
became attacked, as evidenced by ulceration and trophic disturbances. 

An interesting group is formed by those patients in whom trophic distur¬ 
bances and gangrene are the salient features. These are the cases so often 
confused with Raynaud’s disease. The lower extremities are regularly 
involved at some time or other, and it is, therefore, necessary to watch 
carefully for the advent of the typical symptoms in these, so that a correct 
interpretation of the phenomena in the fingers and hands may be made. The 
following two histories will well illustrate. 

VII. More Extensive Gangrene.—The gangrene is usually of very limited 
extent and confined to the tips of the fingers. However, it may progress 
so as to involve the whole of several fingers and be accompanied by such 
signs of circulatory impoverishment as to arouse the fear that the hand or 
forearm may be lost. 


A. K., male, aged twenty-seven years, Russian, was admitted to Mt. Sinai Hospital, 
January 4, 1908. About two years previously he had had severe pain in the middle 
finger of the right hand. The finger became cold, at times very blue, and extremely 
painful. These symptoms persisted for about two months, when he was told to have the 
nail removed. Shortly after this was done the tip of the finger became dry and black. 
After several months the terminal phalanx separated spontaneously, but a wound remained 
which refused to heal. 

For about two months his left hand has been affected, there being excruciating pain in 
the middle finger of the left hand, and the fourth finger of the right hand also being 
somewhat painful. He thinks that the tip of the middle finger of the left hand first became 
dark blue or purple, and lately has become dry and black. 

Physical examination, January 4, 1906, shows that the distal phalanx of the middle 
finger of the right hand is absent, the tip of the fourth finger of the left hand showing a small 
patch of dry gangrene and there is beginning gangrene of the distal phalanx of the middle 
finger. 

Somewhat more than a year later, February 24, 1907, he was again admitted to the 
hospital, presenting evidences of thrombo-angiitis of the left foot. The second toe of the 
left foot had been ulcerated for about three months, and gradually all the toes of that foot, 
except the fourth, became involved in the same process. 

Physical examination, February 24, 1907. Left foot: On the dorsal and plantar sur¬ 
faces of the great toe there are ulcers. A similar condition is found at the tip of the second 
toe and on the plantar and dorsal surfaces of the fifth toe. The skin about the ulcer is 
sloughing and shows no tendency to heal. 

The right foot is negative. The right hand shows an absence of the terminal phalanx 
of the third finger. Both hands are cyanosed. 

March 22. Amputation of the toe. Wound does not heal. 

May 17. Re-amputation through the leg. 

Physical examination, May 20, 1907. The left radial pulse is absent and the artery 
appears to be converted into a hard cord. In the right radial artery a very faint pulse is 
perceptible. The brachial artery seems to be much thickened, although the pulsation is 
good. Ever since amputation of the left leg was done, the stump was painful, discolored, 
bluish, presenting a wound that failed to heal. Finally, on January 2, 1909, the patient 
consented to re-amputation. The author performed the Gritti-Stokes amputation, the 
stump healing kindly. 

January 3, 1909. The tip of the little finger of the right hand presented a small spot 
of gangrene about 1 cm. in diameter. The distal phalanx of the third finger is absent. The 
nail of the fourth finger is deformed and thickened. In the dependent position the fingers 
become cyanotic, with a slight increase in the normal red color. The left hand is normal 
as regards color, but the nail of the middle finger as well as the tip are very much deformed. 

The right radial artery is felt as a cord, and no pulse can be detected; the ulnar artery is 
also pulseless; the brachial pulse is poor. The left radial artery is faint, the ulnar cannot 
be felt, the brachial also is poor. In the elevated position the right hand becomes some¬ 
what paler than the left, but neither becomes very much blanched. 

Lower extremity: The stump is in good condition. The right foot shows evidences of 
development of thrombo-angiitis, the dorsalis pedis and posterior tibial arteries being 
absent, and there are other evidences of involvement of that leg. 


THROMBO-ANGIITIS OBLITERANS—UPPER EXTREMITIES 303 


December 30. The fifth finger of the right hand presents an ulcer at the tip, the result 
of the separation of a gangrenous patch. He says that he has had pain in that finger for 
about three months, and that gangrene set in about three weeks ago. 

February, 1910. . The trophic disturbances, involving the little finger of the right hand 
seem to be progressive. The tip of the finger shows advancing gangrene, the rest of the 
finger is swollen and red. In the dependent position the third and fourth fingers become 
intensely red and slightly cyanotic. Left hand: Here there has been no progression of 
the symptoms. 

February 2, 1910. The little finger of the right hand was amputated (Fig. 51). 



Fig. 51. —Necrosis of the tip of the middle finger of the left hand; results of amputation 
of the fingers of the right. 


This is a good illustration of those cases of thrombo-angiitis obliterans 
in which the symptoms hist make their appearance in the upper extremities, 
are initiated by pain, and followed by trophic disturbances and gangrene. 
In this case the terminal phalanx of the middle finger and the whole of the 
little finger of the right hand were lost. During the evolution of these 
symptoms the disease attacked the left leg, where even greater progress 
was made than in the upper extremities, amputation being the outcome. 
Pathological examination of the vessels of the amputated left limb showed 
the usual lesions of thrombo-angiitis obliterans. 

VIII. Atrophy and Gangrene. —It is rare that gangrene of the fingers 
and hand becomes so extensive as to warrant amputation of the forearm or 
arm. In neglected cases with secondary infection, however, such may be 
the issue. Interesting, indeed, is the occurrence of extensive gangrene of 
one upper extremity and atrophy of the other as results of the vascular 
obliterative process in the following case. 

S. A., male, Russian, examined March 23, 1905, records a typical history of thrombo¬ 
angiitis obliterans of the left lower extremity, finally leading to gangrene, for which the leg 
was amputated August, 1903, and re-amputated September 5, 1903, at the knee. 


304 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Eight weeks before admission there appeared symptoms referable to the same disease 
of the right lower extremity, an ulcer appearing at the inner side of the right heel. On 
March 21, 1905, the right leg was amputated for advancing gangrene of the right foot. 

March 10, 1910. I found evidence of the involvement of the left upper extremity. 
He says that he has had trouble in his left arm and in the fingers and forearm for several 
months, there having been pain in the fingers, followed by swelling and redness. Then a 
bleb appeared at the tip of the index finger, which was incised by a physician. Shortly 
after this the wound became much worse and sloughing took place. About the same time a 
black spot appeared over the back of the middle finger. Neither middle nor index finger 
has improved, and it is for these that he seeks relief. 

After admission the gangrene rapidly spread, the pain becoming excruciating, and the 
forearm was amputated through its upper fourth. 

The ablated forearm (Fig. 52) showed complete occlusion of both radial and ulnar 
arteries. The typical lesions of thrombo-angiitis obliterans were present. 



Fig. 52.—Amputated arm (photographed after fixation) showing extensive gangrene 

of index finger. 

Four years later, April, 1914, the patient was again admitted in a condition of stupor. 
The notes taken read as follows: “ Both legs and the left arm have been amputated. Speech 
is incoherent and there are evidences either of some cerebral lesion or of an arterial lesion 
in the brain. The condition of the right hand is of particular interest. Nowhere is there 
any evidence of ulcer or gangrene. The skin of the right hand is dry and atrophic. The 
fingers have a tapering appearance. The skin has lost its elasticity , the subcutaneous tissues 
have withered , and neither the radial nor the ulnar arteries are palpable. The brachial artery, 
too, gives but the slightest impression of the presence of pulsation.’’ 

Here, then, is a case in which two distinct clinical pictures were evolved 
in the course of the obliterative vascular disease, one exhibiting gangrene of 


THR 0 MB 0 -ANGI 1 TIS OBLITERANS—UPPER EXTREMITIES 305 


an upper and two lower extremities, and the other demonstrating the unusual 
phenomenon of extreme atrophy of both hand and forearm. 

IX. Cases Simulating Scleroderma and Sclerodactyly.— Perhaps most 
interesting of all are those cases in which the vascular occlusion has led, 
by virtue of the effects of malnutrition, to a condition of dystrophy, the clin¬ 
ical picture being akin to that of sclerodactyly. In fact we have had occasion 
to observe a most pronounced example of this manifestation in a patient in 
whom the diagnosis of scleroderma was made by expert dermatologists. 

I. L., aged thirty-five years, was admitted on October i, 1906, with a typical history of 
thrombo-angiitis obliterans of the left leg. There was absence of pulsation in the dorsalis 
pedis and complete gangrene of the second toe, necessitating amputation of the leg. Patho¬ 
logical examination of the vessels of the amputated leg showed the typical lesions of 
thrombo-angiitis obliterans. 

June 29, 1907. He was again admitted to the hospital, complaining of intense pain in 
the right leg which showed the symptoms of ischemia on elevation, redness in the dependent 
position, but no evidence of trophic disorder or gangrene. The patient begged that the 
limb be taken off, and the right leg was, therefore, ablated through the middle third. 
Pathological examinations showed here, too, the typical lesions of thrombo-angiitis 
obliterans. 

December 17, 1909. He entered the hospital complaining of trouble with his right hand 
and arm. For several months he has been unable to use it properly, the muscles having 
become stiffened. He thinks, too, that a marked diminution of the size of the hand and 
arm has taken place. 

On physical examination the picture presented by the right arm is striking. The fingers 
have the typical appearance of the skin in scleroderma. Motion of the distal phalangeal 
joints is markedly impaired in extent. The skin is atrophic and dry and the circumference 
of the fingers of the right hand is distinctly diminished. Both the radial and brachial 
pulses are absent. The brachial artery can be felt as a hard cord, and can be traced as far 
as the axilla. In the axilla there is a distinct pulse. 

The left hand shows no trophic disturbances, no ulcers, but the radial and ulnar pulses 
are absent. The brachial pulse is fairly good. 

X. Cases with Acute Arteritis of Portions of the Radial or Ulnar Artery 
(Migrating Arteritis). —Just as a single or limited number of tributaries 
of the veins of the forearm may be the seat of an acute thrombo-phlebitis, 
and antedate the signs of the deep seated process by months or years, so also 
restricted portions of the radial or ulnar artery may be come suddenly acutely 
inflamed, adherent and thrombosed. An interesting example where that 
portion of the course of the radial artery immediately above the wrist was 
involved, is the following. 

H. S., Russian, male, 38 years old, complained of burning pain in the thumb, index and 
middle fingers of the right hand, also of swelling and reddening over the course of the radial 
artery for the past 4 months. There were no symptoms in any of the other extremities. 

Upon physical examination the right radial artery could be felt as a thickened cord, 
and occluded up to a point 2% inches above the wrist. There was no ischemia, and the 
radial pulse was absent. 

The specimen of the right radial artery after resection showed the following. 

Pathological examination: There was intensive periarteritis and marked thickening of 
the vascular sheath and overlying fascia. When the latter was opened over the groove 
director, the radial artery was firmly adherent and could only be liberated with difficulty. 
About inches were removed. The lower end did not bleed on section, and showed the 
typical lesions of rather advanced thrombo-angiitis obliterans in the brownish stage. The 
upper end of the clot was darkish red, lying in a contracted hut patent vessel 1 inches above 
the wrist. There must have been another thrombotic lesion higher up, since bleeding did 
not occur. It is, therefore, permissible to call the process a migrating one. The absence of 
pulsation in the patent portion was doubtlessly due to a similar occlusive process centrally 
situated. 

Microscopic examination confirmed the diagnosis. 

Another instance of thrombo-arteritis involving the radial and ulnar 
arteries of the right forearm, and a portion of the left radial artery, is illumin- 
20 


306 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


ating in demonstrating the close relationship between the advent of 
circulatory disturbances and tenderness along the course of the right radial 
artery. 

T. G. H., American Gentile, 45 years of age, states that 8 years ago he had had symp¬ 
toms of intermittent claudication of the right leg, followed by similar symptoms of the left. 
The history suggests that there had been migrating phlebitis of the lower extremities. 
Ulceration of the right big toe 5 years ago; subsequently similar symptoms in the left foot, 
and gangrene of both; 2 years ago amputation of both legs at the upper fourth. Three and 
one-half months ago there developed numbness of the tips of the fingers of the right hand, 
with tenderness and vague pain along the course of the right radial artery from the wrist 
to the upper fourth of the forearm, with disappearance of the right radial pulse 1 month 
after the onset of the symptoms. The right ulnar artery disappeared almost simultan¬ 
eously with the right radial. 

Physical examination , January 22, 1923: The fingers of the right hand are colder than 
those of the left; the radial and ulnar pulses absent; moderate ischemia on elevation, 
marked reactionary rubor; tenderness along the lower half of the right radial artery. The 
left radial artery is absent at the wrist, the ulnar pulsates; vasomotor instability of the right 
hand. 


CHAPTER LX 

THROMBO -ANGIITIS OBLITERANS—ASSOCIATED 
ARTERIOSCLEROSIS 

The clinical picture of thrombo-angiitis obliterans becomes confused 
when it is complicated with arteriosclerosis. In most of the cases the patient 
must have had either the insidious or silent form of thrombo-angiitis obliterans 
which developed gradually with only an indefinite history of intermittent 
claudication. These are followed by spontaneous cure so far as evidences of 
impaired circulation are concerned. Later, between the ages of 50 and 65 
or even older, either because of the gradual occlusion of the collateral vessels 
by the atherosclerotic process, or by virtue of a recent thrombosis com¬ 
plicating the arterioslcerosis in the popliteal artery or higher, the symp¬ 
toms of insufficient circulation return, often very rapidly, and gangrene may 
result. In such patients we are apt to find not only pulseless vessels on the 
affected side, but also in the limb which shows no symptoms. 

Or, more rarely do we find thrombo-angiitis obliterans developing rather 
late as far as can be determined by the anamnesis; then a period of temporary 
recovery, followed later on by recurrence of the symptoms in arteries markedly 
sclerosed or calcified. 

The pathological investigation of the arteries in such cases has demon¬ 
strated two lesions side by side, that of the arteriosclerosis with its degenera¬ 
tive sequelae, and that of thrombo-angiitis obliterans (Fig. 124). 

Occasionally we encounter the precocious development of arteriosclerotic 
patches in arteries that are the seat of thrombo-angiitis. We need not 
wonder at this circumstance, since it is not uncommon to find marked 
atherosclerosis in relatively young individuals in whom thrombo-angiitis is 
never a complication. Nevertheless it must be admitted that a predis¬ 
position to vascular disease (vascular mediocrity or inferiority) as it mani¬ 
fests itself in certain cases, seems to express itself both in a susceptibility 
to thrombotic lesions as well as to degenerative ones. Certain it is that 
the autopsy findings in cases of thrombo-angiitis show that the more centrally 



T H ROM BO-A NGIITIS OB LI TERA NS—PA THOLOG Y 


307 


situated arteries do develop a tendency to atherosclerotic lesions even though 
the arteries of the extremities show but little sclerosis. 

For diagnostic and pathological data the reader is referred to the chapters 
on Arteriosclerosis, Pathology, and Diagnosis of Thrombo-angiitis Obliterans. 

Clinically these cases fall into the following groups: 

1. Cases with undiscovered thrombo-angiitis that had been present during 
the early years of maturity (from the ages of 20 to 40), but in which vague 
aches in the limbs, difficulty in walking, and similar symptoms, were insuffi¬ 
cient to lead to a diagnosis. In these patients the disease remained in an 
arrested or non-progressive state. 

2. Cases in which such a latent period as above described is followed by 
a moderate degree of arteriosclerotic change in the arteries of the extremities 
as the individual grows older. 

3; Cases in which the latent thrombo-angiitis is followed by intensive 
arteriosclerosis. 

4. Cases in which either relapsing thrombo-angiitis or bland thrombosis 
in arteriosclerotic vessels leads to gangrene in elderly individuals. 


CHAPTER LXI 

THROMBO-ANGIITIS OBLITERANS—PATHOLOGY 

Thrombo-angiitis obliterans has been previously described by the Germans 
under the name “Spontan-Gangran” and “Endarteritis Obliterans.” In 
1879, von Winiwarter published the results of the pathological findings in 
one case, and reported on obliteration of practically all of the arteries of the 
leg by reason of a chronic proliferative process due, in his opinion, to a new 
growth of tissue from the intima. He, therefore, proposed a new name for this 
condition, namely, “Endarteritis Obliterans.” 

This theory has been accepted by most authors, and even to-day, it is to 
be found in many text books. Somewhat later, Wilonski pronounced the 
opinion that the essential change in the vessel walls was due to a multipli¬ 
cation of the elastic fibers, and proposed the name “Arteritis Elastica” for 
the condition. Perhaps the most important contributions are those of Weiss 
and Zoege von Manteuffel, because these authors placed an entirely new inter¬ 
pretation upon the pathological findings. Basing his paper upon the studies 
of his assistant, Weiss, von Manteuffel suggests that the extensive occlusion 
of the vessels in this disease is dependent upon a primary arteriosclerosis; 
that the obliterative process commences in the popliteal artery, where it owes 
its inception to the formation of a parietal white thrombus; and that by 
virtue of a gradual extension of the parietal thrombus downward, followed by 
organization, a picture resembling an obliterative endarteritis is produced. 
In his cases the veins did not seem to be involved in the process. Von 
Manteuffel comes to the conclusion that the thrombosis is due to desquama¬ 
tion of endothelial cells, and that this occurs where the intima shows most 
advanced lesions of arteriosclerosis, namely, somewhere in the popliteal artery. 

In 1908 the author pointed out that the name, endarteritis obliterans, as 
applied to the clinical picture just described, should be discarded, since the 
occlusive lesion is a thrombotic one, affecting arteries as well as veins of the 



308 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


extremities, and that it is independent of athero- or arteriosclerosis. He 
proposed the name, thrombo-angiitis obliterans , which has now found almost 
universal adoption in English speaking countries. 

Investigations 1 which included a thorough pathological and histological 
study of the vessels in 45 amputated lower extremities, 1 upper extremity, 
and 25 pieces of superficial veins resected and exsected from the lower and 
upper extremitites during attacks of so-called migrating phlebitis, have demon¬ 
strated that when the patient comes to the physician for observation, the 
larger arteries and often the larger veins, are completely obliterated. 



Fig. 53. —Schematic drawing showing the extent of occlusion in the arteries of the lower 
extremities in thrombo-angiitis obliterans. The cross lines represent the points at which 
amputation was done, I indicating the first amputation; II, reamputation. The anterior 
vessels are shown above; the posterior, below. The dotted lines indicate that the vessels 
were not examined. The four sets will be referred to in the text as 53 a, b, c, d, from left 
to right. 


In the Figs. 53? 54, 55? 57? 5 s an d 59 a schematic representation of the 

extent of occlusion in the larger vessels of 29 amputated lower extremities is 

1 Buerger, Am. Jour. Med. Sc., Oct., 1908. Proc. New York Path. Soc., Feb. and 
March, 1908. Int. Clin., Ill, 19th series, 1909. Jour. Med. Res., Nov., 1914, XXI, No. 2. 
Am. Jour. Med. Sc., Feb., 1915, p. 210. 




























TH ROM BO-A NGIITIS OB LI TER A NS—PA THOLOG Y 


309 


shown. Examinations were conducted below the horizontal lines indicated 
in the drawings, and if a second amputation was performed, again in the region 
between two horizontal lines. 

A very extensive obliterative process was found inFig. 53 a where all of the 
larger vessels from the beginning of the popliteal downward, were completely 



in.* am 


Fig. 54.—Schematic representation of extent of occlusion in thrombo-angiitis obliterans; 
referred to as a, b, c, d, e from left to right in the text. 


obliterated. In Fig. 536 upper part of the anterior tibial artery was open 
as depicted, although the posterior tibial and plantars were obturated. The 
sharp lower end of a thrombus is seen in the upper peroneal artery in Fig. 
53c, this being the only one of the larger arteries to remain intact. 

Popliteal thrombosis with patent peroneal and upper posterior tibial 
arteries, is exemplified in Figs. 54a and 55c. In Fig. 546 and c the upper 
extent of the process was detected in each case. More complete involve¬ 
ment of the posterior tibial and popliteal arteries was presented by other 
cases Figs. 54^, 55a and 59 c-d. 

The thrombotic lesion in the popliteal may extend down into the anterior 
tibial, ending abruptly a short distance below the aperture in the interosseous 
membrane (Figs. 56 a and 57a), leaving certain portions of the anterior tibial 
open. 

































310 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Sometimes the posterior vessels except for the plantars are unaffected 
(Fig. 57c) and then again we meet those in which the anterior vessels are 
almost free, except for their most distal branches. Completely patent 
anterior tibial arteries are shown in Figs. 58a and 6; partly open in 58c and d. 

Where the vessels are dotted, their course was not thoroughly examined. 

As a rule, the plantar vessels, dorsalis pedis and many of its branches, 
anterior tibial, posterior tibial, peroneal, and sometimes the popliteal are 
already completely closed, although any one or more of these vessels may 



* IG « 55 -—Schematic representation of extent of occlusion in thrombo-angiitis obliterans, 
(a, b, c, d from left to right). 


escape. One or both the venae comites may partake of the same lesion. 
The obturating tissue is, for the most part representative of, or indicative of a 
healed lesion, or the end-stage of a process, whose incipiency is marked by 
an acute inflammation of the vessel wall, with consecutive, red, occlusive 
thrombosis of the affected vessel. It is only in rare instances that the early 
stages of the vascular lesion are found in the deep vessels, but in superficial 
veins, when they are affected with the lesion migrating or thrombo-phlebitis, 
the early or acute stage of the disease can be studied. 


























TH ROM BO-A NGIITIS OBLITERA NS—PA THOLOG V 


311 


The author has observed what he terms the acute lesions of the disease in 
territories other than the vessels of the extremities, namely, in the spermatic 
artery , in the veins of the spermatic cord; and old lesions in one of the branches 
of the gastric artery in a case of ulcer of the stomach. 

Gross Pathology. —-The deep vessels of the amputated legs regularly show 
an extensive obliteration of the larger arteries and veins. Besides this, there 
are two other lesions which vary greatly in their intensity, namely, the peri- 



Fig. 56.—Schematic representation of extent of occlusion in thrombo-angiitis obliterans, 
(a, b, c, d from left to right). 


arteritis and the arteriosclerosis. The appearance of the vessels on gross 
section depends upon the age of the occluding process. Usually the vessel 
is seen to be filled with a grayish or yellowish mass that can be distinctly 
differentiated from the annular wall of the vessel, and that appears to be 
pierced at one or a number of points by an extremely fine opening, through 
which a minute drop of blood can be squeezed. Such obturating tissue is 
firm in consistency, and does not at all resemble the crescentic or semilunar 
occluding masses typical of arteriosclerosis. The vessel itself is usually con- 





























312 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


traded, so that its wall appears somewhat thickened. This picture is char¬ 
acteristic of arteries or veins which are the seat of a very old obliterative 
process, and is to be found most frequently in the peripheral portions of the 
vessels, although at times this type of lesion may extend throughout the whole 
length of the vessel, from the dorsalis hallucis into the popliteal artery. 


Fig. 



57.—Schematic representation of extent of occlusion 
(a, b, c from left to right). 



As we trace certain of the obliterated arteries or veins upward, we are apt 
to meet with a change in the character of the obturating tissue. Frequently 
it becomes softer, more brownish in color, and terminates abruptly in 
the lumen of an apparently normal vessel; at other times the brownish tissue 
gives way to soft reddish masses which are evidently the results of recent 
thrombosis. In some cases this thrombotic process occupies large portions 
of the vessel’s course; in others, it is of short extent and terminates in a long 
cone of recent thrombus. 

















T H ROM BO-A NGIITIS OB LI TERA NS—PA THOLOG Y 


313 


The veins share equally with the arteries in the lesion of occlusion In 
some cases the veins are more extensively involved than the arteries and this 
is particularly true of the collaterals of the posterior tibial, which are often 
closed when the anterior tibial veins are open. As for the arteries, we usually 
hnd an obliteration of a part or the whole of the anterior tibial, of the dorsalis 
pedis, and dorsalis hallucis, an occlusion of the posterior tibial and plantar 



Fig. 58 —Schematic representation of extent of occlusion in thrombo-angiitis obliterans, 
(a, b, c, d from left to right). 


vessels, with or without involvement of the peroneal. Sometimes the 
anterior tibial is practically normal in its upper half or upper two thirds. 
More rarely a large portion of the dorsalis pedis is open, with the beginning of 
the occlusion in the upper part of this vessel or in the lower part of the 
anterior tibial. 

Besides the lesion of occlusion there are two other striking changes, 
namely, a certain amount of arteriosclerotic thickening and periarteritis. 
Arteriosclerosis is absent in the younger cases; when present, it is never pro¬ 
nounced, except in those rare instances in which the patient has suffered from 
the disease for many years, and has reached the age of 40 or more. As a rule, 


























314 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


we note but a very slight degree of whitening or thickening of the intima, here 
and there, in the patent portions of the vessels. In a very few cases small 
atheromatous patches are present. 

A much more interesting and more important change is the fibrotic thick¬ 
ening of tissues immediately about the vessels. Wherever the vessels are 
occluded, there is apt to be an agglutinative process which binds together the 
artery and its collateral veins, and sometimes also the accompanying nerve, 



Fig. 59.—Schematic representation of extent of occlusion in thrombo-angiitis obliterans, 
(a, b, c, d from left to right). 


so that liberation of the individual vessels by dissection is difficult. The 
adhesive condition is due to fibrous tissue growth, and varies considerably in 
its amount. The periarterial fibrosis varies, sometimes being almost absent, 
at other times so great, that isolation of the vessels or nerves becomes impossi¬ 
ble, and the vascular structures make up one dense rigid cord. 

Histo-pathology.—The lesions may be considered in two stages, first, the 
healed or organized stage, and second, the acute or incipient stage of throm¬ 
bosis. Between the earliest alterations in the deep arteries and veins, and 
































THROMBO-ANGIITIS OBLITERANS—PATHOLOGY 


315 



Fig. 60.—'“Old” occlusion of the fenestrated or cribriform type; large canalizing vessels in 
fairly dense connective tissue filling the lumen of an artery. 



Fig. 61. Elastic tissue formation about the canalizing vessel; a picture that can be 
mistaken for endarteritis obliterans. 






316 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


superficial veins, and the finished product, there are a large number of 
intermediate pictures that illustrate the metamorphosis of the obturating 
clot into the intravascular cicatrix. 

i. Healed or Organized Stage .—The most common lesion is a total oblitera¬ 
tion of the lumina of arteries and veins by connective tissue (Fig. 60). His¬ 
tologically this may be extremely varied in the general appearance, but each 
picture can be interpreted correctly as having its origin in the lesion of occlu- 



Fig. 62.—Absence of elastic tissue in thrombo-angiitis obliterans (orcein stain). The 
umen is filled with old organized clot; no elastic tissue production; below, elastic tissue is in 
arteriosclerotic plaque. 


sive thrombosis. This obturating connective tissue usually harbord 
numerous small vessels, pigment containing hemosiderin, and a fair amounn 
of connective tissue cells. The canalizing vessels, when they become dilateel 
form smaller or larger sinuses, giving the fenestrated or cribriform lesion 
seen on microscopic section of the vessels, or when the canalizing vessel 
becomes eccentrically placed, and sufficiently large, this sinus is responsible 
for the appearances which have been incorrectly interpreted as the product 
of an endarteritis obliterans (Fig. 61). 

Elastic tissue stains demonstrate characteristic differences between this 
process and arteriosclerosis. Thus, the region of the organized clot is almost 
completely free from elastic tissue (Fig. 62). The small amount which is 
present, is concentrically disposed about the new-formed vessels (Fig. 115). 
The abundant elastic tissue formation in the arteriosclerotic plaques is well 
seen in Fig. 63. 


T HROM BO-A NGIITIS OB LI TERA NS—PA THOLOG Y 317 

Still more suggestive and instructive is the finding of various stages of the 
disease in different members of the same vessel sheath. Thus, in Fig. 64 a 
large artery affords a view of the old lesion, as well as one of its venae comites. 
Another accompanying vein, however, is in the “acute” stage of the disease, 
a smaller venule or satellite being in the intermediary stage, where certain 
miliary giant cell foci ’ make their appearance. Such pictures not only 
reveal the thrombotic nature of the disease, but also present an argument in 
favor of the following two assumptions: that the disease begins with an inflam- 



Fig. 63. —Obliterating arteriosclerotic process (orcein). The greater part of the lumen 
is occluded by tissue arising from the intima, and containing the typical elastic tissue found 
in arteriosclerosis; the small triangular clear area in the left part of the lumen contains a 
recent thrombus. 


matory lesion attended with occlusive thrombosis , and that it affects the arteries 
and veins in a sort of relapsing fashion , very much in the same manner as in the 
veins in migrating phlebitis. 

The termination of the occluding tissue in arteries and veins is often seen 
in the form of a rounded, convex projection looking upward (cephalad), and 
lying in practically healthy vessel wall (Fig. 65). At other times, the 
old occluding tissue is capped by an additional clot which rises in pyramidal 
fashion ending by a long tapering extremity. 

2. The Acute or Specific Lesion. —The early lesions are so characteristic 
histologically that their appearances are practically specific for thrombo¬ 
angiitis obliterans and may permit the pathologist to make a diagnosis of 
the disease. They are rarely to be seen in the deep vessels, for the reason 
that patients do not allow amputation until the disease has lasted for months 
or years. However, they can be well studied when these are the seat of the 


318 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


typical migrating phlebitis, and have been shown by the author to be 
identical with the acute lesions in the deep vessels. 

The earliest changes appear to be the usual evidences of an acute inflamma¬ 
tory process involving all the coats of the vessel. The media, adventitia 
and perivascular tissues are infiltrated with polynuclear leukocytes and the 



Fig. 64.—Various stages of occlusion in thrombo-angiitis obliterans; above, a vein; 
just below it, artery in healed fibrotic stage of occlusion; below, two veins; the larger 
recently occluded (acute stage) and the smaller satellite in the intermediate thrombotic 
stage with giant cells. 


lumen of the vessel is completely filled with red clot. In the peripheral 
portions of the clot, larger or smaller foci of leukocytes (purulent foci) begin 
to form, whose growth occurs by virtue of immigration of leukocytes (Fig. 66). 
Certain peculiar giant cell foci develop (Fig. 67), which are characteristic. 
They contain giant cells, endothelioid or angioblasts and numerous broken- 
down leukocytes. These foci then undergo connective tissue replacement. 
The giant cells gradually disappear, numerous small vessels are formed, the 


THROMBO ANGIITIS OBLITERANS—PATHOLOGY 319 

\ 



Fig. 65. —Thrombi in apparently healthy vessels. Upper figure: Conical type of clot, 
there being an accretion or stagnation red clot, over the old obturating organized clot. 
Lower figure: Rounded extremity of the older type of clot ending in apparently healthy 
vessels. 



Fig. 66 .—Acute lesion in internal saphenous vein; on the right, purulent focus; on the left 
remaining crescentic portion of lumen filled with organizing clot. (Giemsa stain,) 













320 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


final product being a fibrous nodule containing vessels and some pigment. In 
the rest of the occluding clot, the organizing process is somewhat different, 
resembling that which characterizes the organization of blood clot in other 
thromboses. 



Fig. 67.—High power appearance of characteristic “miliary giant cell’’ focus in thrombo¬ 
angiitis obliterans. 


In short, the lesions in thrombo-angiitis obliterans are in chronological 
order, an acute inflammatory lesion with occlusive thrombosis, the forma¬ 
tion of miliary giant cell foci, the stage of organization or healing, with the 
disappearance of the miliary giant cell foci, the organization and canaliza¬ 
tion of the clot, the disappearance of the inflammatory products, and the 
development of fibrotic tissue in the adventitia that binds together the 
artery, vein and nerves. 




T H ROM BO-A NGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 321 


CHAPTER LXII 

THROMBO-ANGIITIS OBLITERANS—MORE DETAILED HISTO- 

PATHOLOGY 

For the student of pathology, a more comprehensive account than is 
needful for the clinician may be of value. More detailed knowledge carries 
with it the foundation for a correct interpretation of other occlusive arterial 
lesions. We have only dwelt upon the essential alterations in the previous 
chapter. Here, we shall discuss at greater length, (i) the acute lesions in the 
superficial veins; (2) the acute lesions in the deep vessels; (3) the intermediary 
stages of organization, and (4) cicatrical, ‘‘healed,” or completely organized 
stage. 

The Acute Stage of the Disease.—In superficial veins it has already been 
pointed out that the superficial, that is, the cutaneous and subcutaneous 



Fig. 68 .—Infiltration of the media (below) in a vein and migration of leukocytes into the 

purulent focus (above). 

veins, offered the best material for the study of the earliest or acute lesions 
of thrombo-angiitis. The site of predilection for this thrombophlebitis 
seems to be somewhere in the lower half of the territory of the internal 
saphenous vein, although the external saphenous, saphenous of the thigh, 
median basilic, median cephalic veins of the forearm and foot may also be 
21 




322 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


attacked. Clinically two types of affection manifest themselves, either as 
indurated strands or cords one-half to two, three, or four inches in length or 
as small nodosities. Both of these are the expression of an acute thrombo¬ 
phlebitis, with marked perivascular inflammatory infiltration; in the first 
case, in and about larger veins, in the second, involving minute venules or 
cutaneous tributaries. 



Fig. 69. —Normal organization of red clot on the right, the periphery of a purulent focus 
on the left. In the former new capillary growth, in the latter compressed concentric layers 
of angioblasts (endothelioid), and giant cell formation. 


Even in the cases of migrating phlebitis it is not an easy matter to procure 
material in the proper stage of the disease. It is seldom that the patient 
will consult us at the very onset of the phlebitis, and it is even rarer to be 
able to acquire the veins by extirpation at this time. And that is why 
many of our biopsies were disappointing, yielding lesions already in the 
stage of healing and connective tissue organization. On the other hand, these 
difficulties were of advantage in that we were enabled to obtain veins showing 
many stages of the process and could then synthetize the individual findings 
into a composite picture of the evolution of the disease. 

The general impression obtained from a cursory examination of many 
sections of the affected veins is that we are dealing with an acute inflammation 
of the vessel wall, invasion of the media with polynuclear leucocytes, marked 
reaction on the part of the adventitia, and perivascular connective tissue, 



THROMB 0 -ANGIITIS OBLITERANS—DETAILED HISTO-PA THOLOGY 323 


and an obturating thrombosis, which practically always leads to complete 
closure of the lumen. In the clot which is for the most part red, but also 
contains platelet areas and fibrin, there appear either the typical “miliary 
giant ceir areas, or the precursors of these, collections of polynuclear leuco¬ 
cytes arranged in veritable miliary abscesses. 

For an elucidation of the nature of the pathological process and of its 
metamorphosis into the stages just preceding the healed connective tissue 
product, it may be best to refer to photomicrographs selected from many 
hundreds of sections. In these we will attempt to show that an inflammatory 



Fig. 70.—Greater magnification of Fig. 72; at 2 o’clock the miliary focus; the giant cells 

at 9 and 10 o’clock. 


phlebitis and periphlebitis (or arteritis and periarteritis) are the initial lesions, 
synchronous with the phenomenon of complete vascular occlusion by clot; 
that in the proper evolution of this disease, healing is the rule, in so far as the 
products of the inflammatory stage disappear, and give way to fibrous tissue; 
that in the course of this healing, certain characteristic pictures are evolved— 
such as the miliary giant cell foci—whose raison d'etre can easily be explained; 
and, finally, that the peculiar architecture of the anatomical framework, its 
specificity for thrombo-angiitis, and its purulent foci, all favor the assumption 
that some specific agent, parasitic or bacterial, is responsible for the disease. 

Of all the pictures, that depicted in Fig. 66 and taken from a portion of the 
saphenous vein is the most instructive, for it bears testimony to the presence 




324 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


of an inflammatory lesion. Here we see a vessel filled with clot, a portion of it 
undergoing organization in the normal fashion, the rest occupied by a focus 
of polynuclear leucocytes. Were it not for the rapid changes in the clot, 
such findings would doubtless have been more frequent amongst the many 
vessels examined. But it takes only a very short time for the process of 
organization to completely metamorphose these purulent areas, and develop 
the more usual pictures containing miliary giant cell foci. 



Fig. 71.—Acute stage in superficial vein; at 5 o’clock miliary abscess; rest of lumen filled 
with red clot, in process of “bland” or normal type of organization. 


Such aggregations of cells are not due to fortuitous grouping of the white 
blood corpuscles, for they not only contain more leukocytes than could 
have issued from the intravascular blood stream, but can be seen to owe their 
existence to immigration of cells by way of the media (Fig. 68). Elsewhere, 
the lumen may be ocupied by red clot, in which the typical normal process of 
organization is going on pari passu with certain atypical changes in the pus 
focus (Fig. 69), alterations that lead to the production of the specific pictures 
previously described. 

In the media as well as in the adventitia the evidences of inflammation are 
manifested by intense infiltration with leukocytes (Figs. 68, 70 and 71), which 
seems to be more marked in the superficial (subcutaneous and cutaneous 
veins), than in the deep vessels. Then the fixed cells multiply. Later the 
cellular elements diminish in number, and even disappear, being replaced in 
the media by new vessels, in the adventitia by new formed fibrous tissue. 



TH ROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHLOGY 


325 



Fig. 72.—Acute lesion in vein; on the right, the vein is seen in cross section; on the left, 
a tributary is cut longitudinally and shows an older process. 



Fig. 73. Highj power of Fig. 70; the margin of the inflammatory focus is seen on the 
right; the bland type of organization on the left with the giant cells at the margin. 







326 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In Fig. 72 there is a beautiful example of a vein with the acute lesions. 
Section has been so made that the vessel (on the right) is cut transversely, 
and on the left either strikes the same longitudinally as it makes a sharp bend, 
or possibly goes through a large tributary. The purulent focus is well depicted 
(at 2 o’clock) on the right, with the giant cells clearly defined. Where the 
section passes in a more longitudinal direction and partly tangentially 
through the media, it reveals much older obturating tissue in a solid organized 
form, the inflammatory process in the wall of the vein having disappeared. 



Fig. 74.—High power of a portion of Fig. 71; acute stage illustrating giant cell develop¬ 
ment, and aberrant ingrowth of angioblasts. 


The same vessel seen at another level and reproduced in Fig. 70 will 
clearly illustrate some of the finer details of these distinctive inflammatory 
responses. To the left where the clot is in part of bland variety (red portion) 
organizing capillaries can be seen. The intense cellular infiltration of all of 
the coats of the vein and especially the inner layers of the media is made 
apparent. The margin of a miliary purulent focus, the giant cells and the 
adjacent area of “bland” 1 organization are brought better to view in the high 
power photograph reproduced in Fig. 73. 

Returning to a consideration of the occluding tissue, the two different 
portions merit separate discussion. In the red portion of the clot we see an 


1 Refers to normal and non-specific type of organization. 





THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 327 



Fig. 75.—Acute lesion in superficial vein; media infiltrated; giant cell focus. 



Fig. 76.—High power of Fig. 75; purulent focus with large giant cells; breaking down of 

leukocytes illustrated. 



328 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


orderly penetration of capillary sprouts, the angioblasts forming new capil¬ 
laries (Fig. 69), just as occurs elsewhere in the organization of thrombi, in 
thrombosis of arteriosclerotic vessels, in the accretion clots capping the 
“specific” clots of thrombo-angiitis, or in any clot in which suppuration is 
absent. These areas of organization may occupy a crescentic portion of the 
lumen (Fig. 71) when there is a single purulent focus, or may constitute 
various parts of the clot if several miliary abscesses are present. 

If we carefully study the transition of these typically organized zones 
into the purulent foci, we shall learn why and how the giant cells are formed, 
and will be able to explain the development of the later stages of the pus foci 



Fig. 77.—Giant cell formation in thrombus filling posterior tibial artery, angioblasts 
directly traceable into these cells. 


—the miliary giant cell foci. As the angioblasts approach a purulent focus, 
the cells arrange themselves in compressed, concentrically disposed layers 
(Fig. 74), penetrate the pus foci in a wayward fashion, or form giant cells, 
never showing a tendency to orderly invasion, nor any ability to form vas¬ 
cular sprouts (Figs. 71 and 74). The giant cells must be regarded as abortive 
attempts on the part of the angioblasts to produce new vessels. 

A scrutiny of Fig. 74 will demonstrate how the angioblasts became impo¬ 
tent, as it were, at the periphery of purulent focus, some cells becoming merely 
distorted and unable to enter the leukocytic area at all, others passing in for 
a short distance, or proliferating in loco into a giant cell. 




THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 329 


Figures 75 and 76 illustrate the same phenomena, the giant cell formation 
at the periphery of the infectious focus; and in the high power picture (Fig. 
73) there is clearly indicated the contrast between normal purposeful vessel 
formation in the red clot and the bizarre formation at the edge of and in the 
purulent focus. In Fig. 77, taken from a posterior tibial artery, the abortive 
growth of angioblasts is also illustrated. 



Fig. 78.—Acute lesion taken from the clot of a vein; the greater portion of the area is 
occupied by polynuclear leukocytes; about the periphery of the purulent focus there are 
numerous giant cells. 


Even more striking than in the last sections is the demonstration of these 
facts in Figs. 71 and 74, where a vein in the “acute” stage also contains a 
normally organized crescentic zone and one large miliary abscess. The 
angioblasts can here also be discerned passing into and forming giant cells 
and wandering in irregular, erring fashion amongst the leukocytes. 

The muscle fibers are usually widely separated by the invading cellular 
elements, which are for the most part polynuclear and endothelial leukocytes. 
But where the process has existed for a long time, a large number of new 
formed capillaries still further increase the tissues that separate the muscle 
fibers. These vessels can be traced into the adventitia, which is also consider¬ 
ably increased in thickness, and the fatty tissue in the immediate neighbor¬ 
hood, as in the older specimens, has become more dense and replaced by 
connective tissue. Even the adjacent nerve fibers show thickening of their 
perineural connective tissue and are surrounded by mononuclear leukocytes 
in collections of varying size. 



330 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


To pass in review all the kaleidoscopic appearances that mark the transi¬ 
tion of these characteristic foci into the final, healed connective tissue product 
would be a work of supererogation, for the selected photomicrographs now to 
be shown will suffice to make our argument clear. Unable, then, to organize 
the pus foci, the angioblasts proliferate at the periphery of these. As the 
leukocytes disintegrate (Figs. 76, 78, 79 and 80) and the toxic products are 
absorbed, the atypical distorted angioblasts—now looking like typical 
“endothelioid” cells— together with the giant cells, gradually replace the 



Fig. 79.—Acute lesions; miliary focus in which the process of organization is quite 
advanced, the clear space showing the residual, broken-down polynuclear leukocytes. 
Below there are a number of giant cells, and surrounding the clear space numerous endothe¬ 
lioid or angioblast cells. 


leukocytes from the periphery toward the center, a picture resulting that 
closely resembles miliary tubercles (Figs. 80 and 81). In the center of such 
areas are broken down leukocytes and pyknotic nuclei. No organisms have 
been demonstrable. Still later even the disintegrated nuclei (Fig. 80) dis¬ 
appear, the giant cells atrophy somewhat and a nodule is produced completely 
made up of the altered angioblasts (endothelioid) and giant cells (Fig. 82). 
Although the giant cells may persist for a long time, this tissue is finally 
converted into the fibrillar variety, into which new vessels do penetrate 
(Fig. 83). The rapidity with which this conversion may take place is readily 
understood when those specimens are studied in which, side by side, in 
contiguous tributaries, the older and early process can be followed. 



THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATIIOLOGY 331 



Fig. 8o— Old giant cell focus going on to healing; very few leukocytes remain. » 




332 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 8i. —Miliary giant cell focus resembling tuberculosis in obturating clot found, Jn 
vein of the forearm. Below and on the right side, valves of the vein; above and on the 
left, organization well advanced, tuberculoid focus retaining its characteristic appearance. 





TH ROM BO-A NGIITIS OB LI TER A NS—DE T AI LED HIS TO-PA THOLOG P 


333 




Fig. 82.—Later stage in “acute lesion,” simulating miliary tubercle; endothelioid cells 
and giant cells surrounding focus of disintegrating leukocytes. 


Fig. 83.—Vascularization (in the middle), proliferation of angioblasts and connective tissue 
around the purulent focus (above); older tissue below. 

1 








334 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

The Specific Lesion in the Deep Vessels. —If we turn to a consideration of 
the vessels in which the earliest lesions were best represented, we will be 
apprised of the interesting circumstance that the morphological alterations 
are such as apparently occur only in this disease. Certain foci containing 
giant cells, endothelioid cells, leukocytes and disintegrated nuclei are found 
lying usually in the periphery of a red or mixed clot. These areas strikingly 
resemble tubercles, and, in our experience, have been regularly diagnosticated 
as such by the uninitiated. 



Fig. 84.—Acute lesion in a large artery. The middle coat is infiltrated with leukocytes, 
the clot showing miliary foci. 


The Acute Lesion in the Deep Vessels. —It was possible to study these in 
the arteries and veins of three amputated lower extremities, where extensive, 
acute, inflammatory alterations were present in the popliteal, posterior 
tibial, and peroneal arteries and veins. 

In one of the posterior tibial vessels of large caliber depicted in Fig. 84 
the distribution of at least two purulent miliary foci in the obturating clot, 
and the diffuse inflammatory infiltration of the walls of the vessel are clearly 
represented. Under greater magnification the intensity of the cellular 
invasion and proliferation between the muscle fibers of the vessel wall can 
be well seen in Fig. 85, where the giant cells can also be discerned in the 
obturating thrombus. 




THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 335 



Fig. 85. —Acute lesion in posterior tibial artery. On the left a portion of the media, 
and on the right a portion of the inflammatory clot are shown. Fibers of the media ion the 
left are separated by inflammatory cells (leukocytes). On the right there are miliary 
inflammatory foci with giant cells in the clot. 



Fig. 86. —Acute lesion in deep artery. 




336 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 87. —Acute lesion, a portion of a clot in an artery showing the acute lesion of 
thrombo-angiitis obliterans. At 1 or 2 o’clock the dark area is made up of fibrin; above and 
to the left, giant cells. 



Fig. 88. —Early stage in a deep vein. The media is infiltrated with leukocytes, the lumen 
is filled with clot, in the periphery of which there are miliary giant cell toci. 




TIIROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 337 

In a still larger posterior tibial vessel there is less dispersion of the muscle 
fibers of the media, but the clot itself shows an exquisite illustration of the 
grouping of the miliary foci along its periphery (Fig. 86). 

The formation of the giant cells can be studied in the deep vessels as well 
as in the superficial veins. An illuminating picture is one found in a posterior 
tibial artery, where the purulent focus almost came in contact with the inner 
wall of the vessel. In Fig. 77 the angioblasts can be seen migrating into the 
focus, and pass imperceptibly over into a syncytial body whose termina¬ 
tion is a giant cell. Some of the later stages of organization in, and in the 
neighborhood of the miliary abscesses where the giant cells are taking on 
their older forms are illustrated in Fig. 87. 

The disposition of a number of miliary foci in a deep vein is shown in Fig. 
88 , and the crowding together of the specific elements and reactive response 
into one section of the clot are exemplified in Fig. 89. 



Fig. 89.—Peculiar disposition of giant cells in clot. 


The Intermediate Stage of Healing. —Only a very few examples of the 
types of tissue evolved in the organization of the clot can be offered as examples 
here. Characteristic in the earlier stages are the multiplicity of cells, the 
large amount of pigment, the diffuse distribution of the small capillaries 
interspersed with blood pigment. Later there develops a relative preponder¬ 
ance of young connective tissue with consecutive dilatation of some of the 
canalizing capillaries, and the development of elastic tissue around the new- 
formed vessels pari passu with increasing age. Depending partly upon the 
shape and character of the clot, the fortuitous grouping of the canalizing 
vessels, the eccentric disposition of some clots, the retraction of these from 
the vessel walls, larger or small sinuses may be developed. These give the 
obturating tissue a fenestrated appearance, or make it semilunar on cross- 
section. The latter pictures can be confused with endarteritis obliterans, 
when organization is complete. 

22 


338 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In Fig. 90 the rich cellular substitution of the clot, the interspersed capil¬ 
laries, and the dark areas of blood pigment are the active response which has 
for its purpose the obliteration of the clot with connective tissue. The 
character of the cells is also shown in Fig. 91, where only a part of the organ¬ 
izing tissue has been reproduced. 

Some of the later pictures with the enlarging blood vessels, the disappear¬ 
ance of many of the cells and the increase of young connective tissue can be 
studied in Fig. 92. 



Fig. 90.—Intermediate stage of organization; on the left a portion of the media and the 
internal elastica; on the right, the cellular obturating tissue. 


The formation of larger spaces or sinuses is depicted in Figs. 93 and 94. 
In the former organization is complete, only a part of the vessel wallabeing 
shown. On the right a portion of the occluding tissue with its smaller and larger 
vessels, its capillaries obliterated by connective tissues, and two sinuses of 
moderate size are not unusual appearances (Fig. 93). A higher magnifi¬ 
cation of the tissue in another case, (Fig. 94) shows that these sinuses may 
occasionally be lined with endothelium and filled with blood. Later, how¬ 
ever, their walls are fortified by the deposition of elastic fibers. 

The “Healed” or Old Stage. —For a thorough comprehension of the 
pathology as it presents itself in most of the vessels obtainable from 
an amputated limb— the “old” or “healed” stage is the most instructive. 
The most common lesion is a total obliteration of the lumina of arteries 
and veins by vascular connective tissue. A study of the development 
of this connective tissue shows that the end product may be extremely varied 



THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 339 



Fig. 91 


.—Cellular intermediate stage of the organizing process. 



340 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 92.—High power picture of one variety of end result in the process of organization of 
the clot, the vessels and pigment being striking features. 



TH ROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 341 



Fig. 93.—Fenestrated occluding tissue on the right with two large sinuses; on the left 
a part of the middle coat with the fluted internal elastic membrane running from above 
downward. 




342 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



, . Fig - 94 — A type of obturating tissues enclosing a large blood sinus and smaller capil¬ 
laries. The internal elastic membrane on the left is partly disorganized and well preserved 
on the right below. 



THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 343 


in its general appearance, but that each picture can be interpreted 
correctly as having its origin in the lesion of occlusive thrombosis. Thus 
the vessels may be filled with connective tissue harboring numerous small 
vessels, much pigment containing hemosiderin, with a fair amount of con¬ 
nective tissue cells; or, the cellular elements and vessels may be but sparsely 
represented, dense sclerotic fibrous tissue with but an occasional sinus pre¬ 
dominating. 

Another interesting variant of the terminal stages of occlusion and one 
which is more apt to affect the smaller arteries (such as the dorsalis pedis and 
dorsalis hallucis) is reproduced in Fig. 95. Here the new vessel formation in 



Fig. 95.—Old healed stage in small artery, artery converted into a cord containing dense 
fibrous tissue and vessels. 


the organized clot is striking, and the vascularization of the media can be 
well seen. The penetration of the media by new vessels and the proliferation 
of the small vessels in this coat have been described elsewhere, and need only 
be mentioned here as evidence of the attempt at organization of the clot and 
of the establishment of a supplementary circulation. 

The occlusion of the popliteal artery by the completely organized tissue 
in which every vestige of inflammatory product has been resorbed, a multi¬ 
tude of canalizing channels only remaining, is portrayed in Fig. 96. In 
contrast to this a very small artery may also be completely obliterated into a 
cord of bizarre appearance, because the canalizing vessels have become so 
markedly hypertrophied (Fig. 95). 




344 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 96.—Popliteal artery occluded by vascularized connective tissue, pigment, small 
vessels, and capillaries being features. 




TH ROM BO-A NG 1 IT IS OBLITERANS—DETAILED HISTO-PATHOLOGY 345 



Fig. 97.—Old type of organized clot showing cicatricial contraction of the connective 
tissue, and occlusion and compression of the cellular elements, also secondary thickening of 

the intima. 


346 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


With increasing age, changes in the intima may occur that show themselves 
as diffuse thickening, and the vessels contract about the obturating tissue, 
the latter becoming more and more firm (Fig. 97). This cicatrization may 
go on to such an extent as to give confusing products, in that the hypertrophy 
of the intima may lead to erroneous interpretation. The contraction of the 
obturating tissue mass, the enlargement of the intimal layers and the diffuse 
fibrosis about the vessels extending well into the fatty tissues about the arteries 
can be studied in Fig. 98. 



Fig. 98. —Contracted type of closed artery. The lumen is narrowed and filled with 
fibrotic tissue. The intima shows hyaline degeneration and is thickened following the 
thrombotic process. 


In the older stages in which there is but a sparse distribution of the cells in 
the cicatrizing mass, the veins are apt to show less contraction than the arteries. 
So in a vein shown in Fig. 99, the irregular sinuses that canalize the occluding 
mass are in sharp contrast to the more rigid and contracted process in the 
cribriform arterial sections shown in Fig. 100. 

Again in the artery in Fig. 101, where a central lumen is simulated by a 
narrow canalizing channel, the retraction of the internal elastica with 
corresponding constriction of the artery is well shown. Fig. 102 is an interest- 


THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 347 



Fig. 99. Old sclerotic occluding tissue in a vein. 



Fig. too. Old or healed type of lesion with large canalizing vessels. 



348 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. ioi.—O bliterating tissue, old variety in dorsalis pedis, can be mistaken for “endarter¬ 
itis;” old connective tissue, canalization; only slight vascularization of media. 



Fig. 102.—“Old” occlusion in artery simulating “endarteritis obliterans;” eccentric¬ 
ally situated large canalizing vessel (below) crowding rest of tissue to one side (above in 
illustration). 





THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 349 



Fig. 103. —Lesions of the media in medium sized arteries; many capillaries with or 
without slight perivascular lymphoid infiltration in the media; penetration ot the internal 
elastic lamina by vessels which enter rather old typical occluding tissue. 



Fig. 104. —Longitudinal section of an artery containing termination of organized clot; 
to the left the arterial walls are normal, collapsed and in contact; to the right, occluding 
tissue. 




350 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


ing illustration of an eccentrically placed canalized channel that crowds the 
organized clot into the small crescentic mass on the right and is an example of 
the formation of pictures that can be mistaken for endarteritis obliterans. 

The change that is left in the media in the healed stage, besides connec¬ 
tive tissue infiltration and atrophy, is the diffuse invasion with new formed 
vessels (Fig. 103). Although this process is most pronounced in thrombo¬ 
angiitis obliterans, it can be also observed in atherosclerotic processes, 
whenever secondary thrombosis occurs, or whenever there is marked degener¬ 
ation, calcification or bone formation in the walls. 



Fig. 105.—Termination of the red clot in a vein. It is adherent at 3 o’clock, and in the 
media at this site there is inflammatory infiltration. 

Terminations of the Occluding Tissue.—Studying some of the termina¬ 
tions of the occluding tissue in arteries and veins, we not infrequently 
encounter a rounded convex projection looking upward (cephalad), abruptly 
ending the obturating plug, and often lying in and just below an apparently 
healthy vessel wall (Fig. 65). At other times the old occluding tissue seems 
capped by a more recent pyramidal or tapering clot, which appears grossly 
and microscopically to be deposited by mere accretion (stagnation clot). 
When we view the former type, as illustrated in the longitudinal section 
(Fig. 104), we can well understand the nature of the pathological change. 
Here there can be no doubt as to the thrombotic nature of the process. 
The accretion or stagnation clots, on the other hand (Figs. 105, 106, and 
107), present a somewhat different picture, not varying from that of throm¬ 
bosis and organization induced by other causes. 




THR0MB0-ANGI1TIS OBLITERANS—DETAILED HISTO-PATHOLOGY 351 


Fig. 106.—Bland termination of accretion clot in vein with healthy wall. 


(See Fig. 105.) 





352 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 107.—Termination of clot in an artery the seat of atherosclerotic disease; good 

example of associated lesions. 




T H ROM BO-A NGI IT IS OBLITERANS—DETAILED HISTO-PATHOLOGY 353 


In Fig. 104 the rounded termination of the obturating mass is seen lying 
in a vessel cut longitudinally, and whose walls are collapsed just beyond the 
organized clot. The latter presents the usual picture of the old stage with 
connective tissue vessels and pigment. A parietal termination in a vein is 
seen in Fig. 108. 

The accretion clot may be either abruptly separated from the specific, 
or may pass imperceptibly into it. When the latter is the case, the tapering 
termination may be found adherent to the wall in places, and it is there that 
evidences of the inflammatory nature of the process may still be present. 
In Fig. 105 such infiltration of the media and intima is seen where the clot is 



Fig. 108.—Termination of obturating tissue in a vein in parietal form. 


attached. If the media be infiltrated with migrating and polynuclear 
cells, we may conclude that the specific inflammatory process has extended 
into and emerges imperceptibly into the accretion clot. If the organizing 
process is the typical bland one, no such reaction in the media can be noted. 

Fig. 106 shows sections made somewhat nearer the apex of the clot, the 
vessel being absolutely healthy in this region. 

When such a termination occurs over an atherosclerotic or thickened 
intima, confusing pictures may result after organization has taken place 
(Fig. 107).. 

In rare instances terminations of the clot may adhere in a parietal fashion 
to the walls of the vessels, as shown in the vein in Fig. 108. 

23 




354 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The Pathology of the Relapsing Lesion.—Not only is the process a migrat¬ 
ing one both in arteries and veins, but all of the constituents of a sheath may 
not be simultaneously affected. An old advanced lesion may be found in an 
artery or vein, an acute lesion in contiguous vessels. The finding of various 
stages of the disease in different members of the same vessel sheath is exceed¬ 
ingly instructive. This is well illustrated in Fig. 64. 

Thus in Fig. 109 a large artery affords a view of the old lesion, as well as 
one of its venae comites. Another accompanying vein, however, is in the 
“acute” stage (Fig. no) of the disease, a smaller venule or satellite being in 



Fig. 109. Old sclerotic occluding tissue in thrombo-angiitis obliterans; a high power 
magnification of this vessel being reproduced. (See Fig. 64.) 


the intermediary stage, where certain “miliary giant cell foci” make their 
appearance (Fig. m). Such pictures not only reveal the thrombotic nature 
of the disease, but also present an argument in favor of the following two 
assumptions: that the disease begins with an inflammatory lesion attended 
with occlusive thrombosis, and that it affects the arteries and veins in a sort 
of relapsing fashion, similar to that which occurs in the veins in migrating 
phlebitis. 

Recurrences are found also in the deep vessels. In the popliteal vessel 
seen in Fig. 112, evidences of thromboses are found. The whole artery was 
doubtlessly affected by the acute process a long time since, for the lumen was 
filled with the old type of organized tissue, many capillaries and large blood 
sinuses, and thick walled canalizing vessels. One of these daughter canalizing 


T H ROM BO-A NGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 355 



Fig. i io. —Acute stage in another of the veins seen in Fig. 64. 






356 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Pig. ii 



i.—Miliary foci in an acutely inflamed vein in same sheath with preceding. 

Fig. 64.) 


(See 




THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 357 


Fig. ii2 


.—Relapsing acute stage in an artery already occluded and in the old stage 
on the left, giant cell focus. 




Fig. i 13.—High power of Fig. 112 




358 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


arteries shows the acute process within its walls, and a miliary giant cell 
focus. A high power view of this focus is seen in Fig. 113. Thus the com¬ 
bination of an old healed lesion with a recent superimposed acute inflamma¬ 
tory one in a daughter canalizing vessel is beautifully shown. 

A similar instance of combined old and recent lesion in the peroneal 
artery is depicted in Fig. 114. Here the crescentic mass to the left in the 
picture shows the healed connective tissue stage, and in the eccentric lumen 
that is left, recent thrombosis, acute inflammation, and miliary giant cell foci 
are present. 



Fig. 114.—Combined old lesion and recent acute lesion in an artery (peroneal). The 
peripheral portion of the obturating tissue is composed of vascularized connective tissue. 
On the right, the greater portion of the lumen, however, is occupied by a more recent clot 
with miliary foci. 


The Elastic Tissue in Thrombo-angiitis Obliterans.—What information 

can be obtained from a study of specimens stained for elastic tissue? 

Characteristic of the early stages of the metamorphosis of the obturating 
clot is the absence of elastic tissue, and also the absence of the excessive 
reduplication of the internal elastic layer so characteristic of arteriosclerotic 
processes. As the canalizing vessels become older, however, new formed 
elastic tissue disposes itself about them (Fig. 115) in concentric layers. The 
scant development of the elastic tissue in a popliteal artery completely filled 
with organized clot is seen in Figs. 116 and 117, where but the faintest indica¬ 
tion of new elastic fibers is seen about some of the canalizing vessels. Where, 
however, there are small complicating plaques of arteriosclerosis, there the 


THROMBO-ANGIITIS OBLITERANS—DETAILED HI ST O -PATHOLOGY 



Fig. i 15. —Elastic tissue stain of section of vessel shown in Fig. 101. 


360 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 116.—Occluding tissue devoid of elastic fibers in the popliteal artery 






TH ROM BO-ANGIITIS OBLITERANS—DETAILED HISTO-PATIIOLOGY 361 



Fig. ii 7.—Elastic tissue but sparsely represented about the vessels of the occluding tissue 

in a vein. 




362 


CIRCULATORY AFFECTIONS OF TIIE EXTREMITIES 


Fig. 



118.—Absence of elastic tissue in the clot; small atherosclerotic patch^below in'fthe 

intima of the artery. 



Fig. i 19.— New lumen found in organized clot in vein simulating endarteritis obliterans 

(elastic tissue stain). 






TH ROM BO-ANGIITIS OBLITERANS—DETAILED IIISTO-PA T HO LOGY 363 

corresponding hyperplasia and duplication of elastic lamina take place 
(Fig. 118). 

Serial sections stained with the elastic tissue method demonstrate clearly 
that the occasional pseudo-lumina (Fig. 119) found in arteries of thrombo¬ 
angiitis obliterans are but expanded or eccentrically placed canalizing sinuses 
which divide up into subsidiary branches and are traceable (Fig. 120) into 
numerous smaller canalizing vessels at different levels. 



Fig. 120. Septum formation due to the eccentric position of the two large canalizing 

sinuses. 


In Fig. 120 the elastic tissue disposed about the two sinuses separated 
by a septum stamps these as new formations. Elsewhere they are found to 
divide into smaller canalizing vessels. 

Other sections, such as are seen in Figs. 121 and 122, further demonstrate 
the new formation of elastica about a canalizing vessel. 

Where, however, the lesion is one of long duration (years), a secondary 
thickening of the intima takes place with corresponding proliferation of 
elastic fibers that must not be confused with arteriosclerotic processes 
(Fig. 123). 

True atherosclerotic plaques in which the elastic fibers are disposed more 
or less parallel with the internal elastica lamina and encroaching upon the 
lumen of the vessel may occur, for the two diseases may he associated. This 
is seen in Fig. 124, where such an atherosclerotic plaque occupies the cres¬ 
centic portion of the right part of the lumen, whilst the occluding mass of 
thrombo-angiitis obliterans completes the recess left. 



364 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 











TH ROM BO-ANGIITIS OBLITERANS—DETAILED IIISTO-PATHOLOGY 365 



Fig. 123.—Relative absence of elastic fibers in the organized clot; secondary hyperplasia 
of the intimal elastica in the artery below. 



366 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 124.—Old type of occlusion at site of an arteriosclerotic plaque on the right. 


THROMBO-ANGIITIS OBLITERANS—DETAILED HISTO-PATHOLOGY 367 



Fig. 125.—Elastic tissue stain showing old lesion in arteries and venae comites; also 
picture in vein simulating endarteritis obliterans; on the left and right, arteries; in the 
middle two veins, the left with small, the right of the two with a large canalizing channel. 



Fig. 126.—Fibrosis of perivascular tissues binding the two vessels above together; 
endarteritis and endophlebitis here simulated. 






368 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Of great value is a study of those sections that include a number of the 
larger obliterated vessels, as is seen in Figs. 125 and 126. Many of these 
will exemplify the secondary sclerotic intimal changes 1 that occur long 
after the occlusion has taken place; and further, they will demonstrate the 
fibrosis that binds the arteries and veins together, being the sequel of an 
inflammatory process extending from the adventitia. Fig. 126 shows 
beautifully how the two vessels on the right are encased in a dense fibrous 
sheath, whilst the large canalizing lumina suggests endarteritis obliterans 
rather than thrombo-angiitis obliterans. No wonder then that these lesions 
should so long have been misinterpreted. 


CHAPTER LXIII 

THROMBO-ANGIITIS OBLITERANS—PATHOLOGY IN LETHAL 

CASES 

The autopsyTnaterial studies by the author was obtained from c^ses that 
died after amputation or from other causes. In the former, exitus was due 
either to pulmonary embolism, embolism of the mesenteric arteries, or to 
accidental causes. 

Little .jsjmown regarding the participation of arteries other than those 
of the extremities in the characteristic process. The author has observed 
the “old type” of occlusion in the spermatic artery; and in a branch of the 
gastric artery leading to a callous ulcer of the stomach. Since but a small 
amount of material was at hand, it would be audacious to assert positively 
that the lesion was identical with that of thrombo-angiitis. However, 
recently the typical “acute” lesions were found in the spermatic vessels of 
the cord. 

In a young man who consulted the author for a subacute enlargement of the testis, 
epididymis and cord, the diagnosis of tuberculosis or thrombosis of the vessels of the cord 
was made. Orchidectomy yielded an interesting specimen in which most of the veins 
(spermatic) of the cord and tributaries about the testis, were thrombosed. Microscopic 
examination revealed the typical “acute lesions” in many of the vessels. 

The literature is practically devoid of reliable information on this point, 
so that autopsy material is highly desirable for enlightenment. But few 
data could be gathered since only 3 autopsies 2 were done on the cases under 
the author’s observation. Great care must be exercised in interpreting the 
significance of the endarterial lesions evidenced by necropsy, since years had 
elapsed in 2 of the cases since the amputations of the lower extremities had 
been performed, during which time intercurrent affections, atherosclerosis 
and secondary thromboses could play a role in producing the final anatomical 
and pathological results. Because of the paucity of such records in the 
literature, however, it may be valuable to give in detail these findings, even 
though a a final and authoritative interpretation of their importance and 
meaning may not be permissible from the meager data at hand. 

1 See also similar alterations in the veins. 

2 Autopsy material and findings in an additional case, in which the fatal outcome was 
accidental and due to hemorrhage in the wound were put at the author’s disposal through 
the courtesy of the Pathological Laboratory, Mt. Sinai Hospital. 



THROMBO-ANGIITIS OB LI TER A NS—PA THOLOG Y IN LETHAL CASES 369 

The fact that in the autopsy material at our disposal, the lesions of 
thrombo-angiitis obliterans were confined to the vessels of the extremities, 
might lead to much speculation and critical query. It would seem that local 
predisposing factors must needs be requisite for the special susceptibility of 
these vascular territories. In the present state of our knowledge we think 
it unwise to attempt to give explanations for all of the many seemingly 
inexplicable circumstances that surround this interesting malady. That the 
arterial channels affected by thrombo-angiitis become, or are inherently pre¬ 
disposed to atherosclerotic changes as well, seems proven both by autopsy 
material as well as through our studies of the amputated limbs. Where 
reamputation is done years after the more distal part of the limb has already 
been removed, more marked atherosclerosis is found. Or, when the second 
lower extremity requires amputation years after the first, atherosclerotic 
changes may be found that were absent during the earlier years of life; they 
may be slight or marked in degree. 

The fatal termination in some of the cases may be accidental, dependent 
on the cardiovascular system, or may be preceded by a state of malnutrition 
and asthenia occasionally observed in cases of extensive atherosclerotic 
disease that have already lost both lower extremities. 

The following grouping is now permissible in consonance with the author’s 
experience: (i) the fatal cases in which death may be attributed to the 
operation, or some sequela of the disease itself (accidental); or (2) cases with 
asthenia and slow termination, possibly with cerebral arterial involvement. 

1. Accidental Exitus.—As accidental we would designate the lethal out¬ 
come in cases that die from cardiac failure after operation, from hemor¬ 
rhage or from pulmonary embolism. The author has personal records of but 
2 cases of embolism with fatal termination after Gritti-Stokes amputation. 
In one there was pulmonary embolism with sudden exitus, in the other, 
mesenteric thrombosis or embolism. Cases collected elsewhere 1 afford 
instances of accidental complications and death, such as fatality from hemor¬ 
rhage at the site of the ablation. In one such instance the autopsy material 
studied by the author again confirmed previous observations in the finding of 
atherosclerosis of some of the larger vessels and in the absence of the thrombo¬ 
angiitis process outside of the peripheral territories. 

Case 1. Thrombo-angiitis; precocious atherosclerosis; coronary artery 
disease; sudden exitus. 

F. K., male, aged 24, when admitted November 5, 1907, stated that 1 year ago he had 
severe pain in the left big toe; this recurred 2 weeks ago, and has grown progressively worse; 
the foot is swollen, red, and tender; for the past 2 days the big toe has become bluish in 
color; intermittent cramp-like pains in the calf of the right leg have also been experienced. 

On physical examination the left foot is seen to be very edematous up to the ankle; 
tenderness of the big toe and cyanotic discoloration; slight erythromelia of the toes of the 
right foot. 

Nov. 6, 1907, incision and drainage of cellulitis of left foot; Nov. 8, amputation of left 
big toe for gangrene; Dec. 19, left dorsalis pedis pulse absent , right present. Because of the 
failure on the part of the wound to heal, amputation at the left knee was resorted to, Mav 8, 
1908. ’ 

Further examinations May 27, 1908, revealed absence of right dorsalis pedis and posterior 
tibial beats, and slight ischemia of the right foot upon elevation; July 15, still absent right 
dorsalis pedis and posterior tibial pulses, but good pulsation in the right popliteal artery; 
ulceration of the left stump; Aug. 20, absent left popliteal, only faint popliteal right, and 
pain in the right foot and calf. 

• i 5 ^ Pky sica l examination Jan. 23, 1909, there was marked erythromelia of the entire 
right foot, edema of the first and second toes, which were also in a state of trophic distur- 

1 Studied with the permission of Drs. Mandlebaum and Libman of the Pathological 
Department, Mt. Sinai Hospital, N. Y. C. 

24 


370 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


bance. March i, 1909, amputation of the right leg at the middle third for impending 
gangrene. 

The patient was lost sight of until May 2, 1911, when he returned to the hospital because 
of the presence of a painful sinus on the right stump which had persisted for 3 months. 
Both femoral pulses were good at this time, but the right popliteal had completely disap¬ 
peared. Because of the pain and ulceration, Gritti-Stokes amputation of the right thigh 
was performed May 29, and, although the patient had engaged in conversation with the 
nurse following the operation, was shortly afterwards found dead. 

Histologic examination of the vessels from the right and left legs established the diag¬ 
nosis of thrombo-angiitis obliterans. 

Autopsy Diagnosis: Thrombo-angiitis obliterans atherosclerosis of the coronary arteries, 
interstitial myocarditis. 

Heart—Rather smaller than normal; tricuspid orifice about normal, tricuspid 
flaps show no thickening; right ventricle outflow tract dilated, wall very thin 
measuring about 2 to 9 mm. Pulmonary valves show no abnormality; few fatty plaques 
at the origin of the pulmonary artery; left auricle endocardium somewhat whitened; 
mitral valve shows distinct thickening at its edges; left ventricle dilated; heart muscle very 
brown, measures 8 mm. in thickness and throughout it yellowish areas of degeneration can 
be seen, some of which look fatty and other areas of a more or less circumscribed fibrosis 
Such lesions can only be found in the wall of the left ventricle, and not in that of the right; 
left coronary artery is normal for about 1.5 cm. from its origin, when the main branch 
running down to supply the left ventricle is found to be more or less filled by fibrous, yellow¬ 
ish white substance, which is adherent to the wall and divides the lumen of the vessel into 
two very small parts (recanalization?). This fibrous process in the lumen of the vessel can 
be traced down for about 3 cm., when the vessel is lost. The right coronary artery and 
veins show no such change. At the point of origin of the right coronary artery there is an 
atherosclerotic plaque on the right posterior sinus of Valsalva, which encroaches upon the 
lumen of the orifice of the right coronary to such an extent as to very markedly obstruct it; 
in fact, the orifice is only pin-point in size. There are numerous pin-head and slightly 
larger atherosclerotic patches scattered diffusely beneath the intima. 

Lungs—Both lungs show very dense adhesions at the apices and along the posterior 
border. 

Liver—About normal in size, dark reddish brown in color. 

Spleen—About one and a half times normal size, shows the presence of 2 depressions 
beneath the cortex, which on section are found to be healed infarcts, and consist of fibrous 
tissue containing some yellowish pigment; capsule slightly thickened and has a few adhe¬ 
sions scattered over it. On section, the organ is of a bright red color, very soft and the 
Malpighian bodies stand out prominently; splenic vessels show no changes. 

Kidneys—About normal in size; capsules strip easily. The cortex shows a few smaller 
and larger reddish depressions, evidently healed infarcts. On section, the cortex and 
medulla of normal proportions, markings fairly distinct. 

Microscopic examination of the coronary arteries presents the typical 
picture of arteriosclerosis. In short, marked lesions of atherosclerosis in 
the coronary arteries, but nowhere any evidences of thrombo-angiitis 
obliterans in the vessels examined. 

Case 2. Thrombo-angiitis; extensive atherosclerosis; bland thrombosis in 
aorta, coeliac axis, superior mesenteric arteries; exitus. 

In the case B. D., aged 21, male, a typical Gritti-Stokes amputation of the left thigh 
was done July 19, 1916, and the usual lesions of thrombo-angiitis obliterans found in the 
vessels of the extremity, even at the site of ablation in the popliteal artery. July 21, the 
patient complained of intense pain in the abdomen, and there was marked rigidity of 
the abdominal wall. Per rectum a boggy mass could be felt, and the patient was in great 
distress because of the pain and distension. The diagnosis of mesenteric thrombosis was 
established, and at operation July 22, gangrenous gut was revealed; exitus. 

Author’s notes on viewing autopsy July 24, 1916: Extensive thrombosis of the coeliac 
axis and of the superior mesenteric artery; gangrenous gut; the femoral artery and external 
iliac on the side of the amputation, about 1inches above Poupart’s ligament thrombosed. 
In the external iliac there is a stagnation or accretion thrombus descending to meet the top 
of the old thrombus; in the femoral or possibly the distal part is an extension from the old 
clot in the femoral (accretion and stagnation). 

In the aorta, mural thrombi some extending into the coeliac axis and the superior mesen¬ 
teric; numerous infarcts in the spleen, in the kidneys, and infarctions of the heart. 


TH ROM BO-ANGIITIS OBLITERANS-PATHOLOGY IN LETHAL CASES 371 


Autopsy July 22 Body is that of a young adult male; no icterus or petechia;; moderate 
rectus^nusde ^ ^ haS be6n amputated above knee » surgical incision through right 

Heart-on the anterior surface of the right auricle, near the base, milk-spot the size of 
a five cent piece, right heart moderately dilated; the tricuspid and pulmonary orifices 
normal mitral shows few small yellowish, atheromatous patches. In the inner leaflet of 
the posterior wall of the outflow tract, near the aortic orifice, is an irregular, grayish patch 
which upon section, appears to be diffuse scarring. Another similar patch is found in the 
muscularis near the apex. Coronary vessels show very marked atheroma; entire intima 
presents numerous raised patches. Here and there, however, are small button-like eleva- 
normal n ° duleS m the media of the vessels over which the intima appears perfectly 

en - i A C in T tim t Studded with irre g ular > yellowish, atheromatous 
patches (ordinary atherosclerosis). In the upper part of the arch near the origin of the 
great vessels are two button-like patches, about 2 cm. in diameter. On section, these are 
situated in the media and consist of dense fibrous tissue, the intima and adventitia cover- 
ing them not being involved. The fatty atheromatous changes in the intima extend all the 
way down the thoracic and abdominal aorta on its posterior wall, also on the posterior wall 
near the site of the cceliac axis, is a thickening of the intima similar to that described in 
the aortic arch, which has apparently ulcerated into the lumen. The base of the ragged 
ulcer is covered by a layer of blood platelet thrombus. About 1 inch below this, also on the 
posterior wall of the vessel, is a still larger patch which is ulcerated. The base of the ulcer 
is also covered with blood platelet thrombus which extends down into the common iliac 
artery, occluding it completely at about iK inches from the bifurcation. The left common 
iliac artery is closed by red thrombus. In the upper portions of the femoral artery, how¬ 
ever, the thrombus again becomes blood platelet in type, and on the posterior wall of the 
femoral artery is a marked fibrous thickening, apparently disease of the vessel. The supe¬ 
rior mesenteric artery is closed at the beginning by a blood platelet thrombus, lower down 
by a red thrombus. The mesenteric vein is filled with red thrombus. One of the main 
branches of the splenic artery is also filled with a blood platelet thrombus. 

Liver—moderately enlarged, cloudy parenchyma. 

Spleen about 1 34 times its normal size; center portion presents a large, firm, yellowish, 
anemic infarct similar to the infarct seen in subacute bacterial endocarditis. 

Kidneys—normal in size, capsules strip with some difficulty, surface smooth; intense 
congestion of the parenchyma. 

Adrenals and pancreas—negative. 

Gastro-intestinal tract—intense congestion of the serosa of the stomach and small 
intestines; complete gangrene of the terminal 4 feet of ilium. 


Microscopic examination of the superior mesenteric, common iliac, 
femoral, external iliac, abdominal and thoracic aorta showed the typical 
lesions of arteriosclerosis with varying degrees of thrombosis (parietal and 
occlusive) of the mechanical type; nowhere lesions of thrombo-angiitis 
obliterans. 

2 . Cases with Slow Termination. —Just as in certain cases extensive 
aortic thrombosis was found, so here the mental condition antedating exitus 
would suggest the possibility of thrombosis of bland or specific (thrombo¬ 
angiitis) type in the territory of the cerebral vessels. Such a case is the 
following. 

Case 3. Amputation of both lower extremities and one upper; duration of 
disease 10 years; exitus with cerebral symptoms. 


S. A aged 35, male (see Chapter on Thrombo-angiitis Obliterans of the Upper Extremi¬ 
ties), when examined August n, 1903, reported trouble in the left foot, 3 years previously, 
oince then there were attacks of pain in both feet. 

For the past 2 days (Aug. n) the left foot has been painful, particularly at night, so 
it now he is unable to stand. His clinical course may be divided into four stages; 


/ x - — 7 *«»*«*. diuicoi luuisc umy ue uiviaea into iour stages; 

U) gangrene of the left leg; (2) gangrene of the right leg; (3) gangrene of the left forearm; 
and (4) cerebral symptoms leading gradually to exitus. 

I * Amputation of the Left Leg .—Examination reveals early signs of gangrene of the great 
toe o. the left foot. Aug. n, 1903, amputation of left leg; Aug. 15 to Sept. 2, no tendency 
to heal sloughing marked; Sept. 5, reamputation through the knee; Sept. 22, again necrosis 
ol the flaps; Oct. 3, reamputation through the middle of the thigh. A thrombus 4 inches 
m length was extracted from the femoral artery; Oct. 24, wound healed 


372 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


2. Amputation of the Right Leg .—March 23, 1905, says he has been suffering for 8 weeks 
with pain in the right foot. An ulcer developed on the inner side of the heel, and recently 
this region has become black. 

Examination reveals a gangrenous area over the right heel; March 31, 1905, amputation 
through the upper third of the right leg; March 15, 1907, because of recurrence of gangrene 
in right stump, reamputation through lower third of thigh; June 13, 1907, patient insists 
upon leaving hospital, although bare bone with suppurating sinuses can be still detected. 

3. Amputation of Left Forearm .—March, 1910, says that since 6 weeks has had severe 
pain in index and middle fingers, which gradually became swollen and red; after the incision 
of a bleb at the tip of the index finger, gangrene of index and middle fingers set in. Notes 
made March 14, 1907, called attention to the absence of the left radial pulse and cyanosis 
of the hand. March, 1910, amputation through forearm for gangrene. 

4. Exitus with Cerebral Symptoms .—April 14, 1914, patient admitted to hospital in 
stuporous condition. There had been no apoplexy and no signs of palsy. Physical examin¬ 
ation—patient incoherent in speech; talks in mumbling unintelligible manner; pupils are 
equal and react to light; right upper lid is ptosed; right radial pulse absent (the left forearm 
has been amputated); left thigh stump contains a sinus; from the right stump dead bone 
protrudes; April 24, 1914, condition unchanged; April 29, temporal pulse weak; marked 
asthenia; exitus. 

Case 4. Amputation of both lower extremities for thrombo-angiitis obliterans; 
obliteration of the brachial arteries with a clinical semblance of scleroderma and 
sclerodactyly, lethal outcome, autopsy showing thrombosis of a portion of the aorta. 

I. L., male, aged 35 years, examined Oct. 3, 1906, said he had always been well. Ten 
months ago he began to experience pain in the left ankle shooting into the toes (acute stage 
of the disease in the deep vessels, plan tars and posterior tibial behind the ankle?). At first 
this was intermittent but soon became constant. He became progressively worse so that 
he was then confined to his bed for several months because of the pain. He was in the 
hospital a few months previously when amputation was suggested, which was refused. 
About 1 month ago the toes of the left foot became dark in color, exceedingly painful and 
then an ulcer developed on the dorsum. 

Physical examination: A rather poorly nourished man; good radial pulsations. The left 
foot is the seat of gangrene involving the second toe, which is black. The other toes are 
deeply cyanotic, partly anesthetic. Near the root of the second toe on the dorsum there is 
a sloughing ulcer the size of a quarter, at whose base a tendon is exposed. The dorsalis 
pedis pulse is absent. Lymphangitis extends upwards to the mid-calf. The popliteal and 
femoral arteries pulsate. 

Oct. 3, 1906, osteoplastic amputation of the left leg through the mid-calf region. Necro¬ 
sis of the flaps and bone, with healing, Nov. 17, after removal of dead bone and sloughing 
skin. 

Pathological examination of the occluded vessels showed the typical lesions of thrombo¬ 
angiitis obliterans. 

In June, 1907, the pain in the right leg became so intense, that although gangrene had not 
occurred, the patient begged for amputation of this leg too. Therefore, July 1, 1907, an 
osteoplastic amputation was done, but because of unsatisfactory healing reamputation 
had to be resorted to, July 15, 1907. 

Pathological examination of the obliterated arteries showed both the old and acute 
lesions of thrombo-angiitis obliterans. The posterior tibial contained miliary giant cell foe 
characteristic of the disease. 

Dec., 1909. The patient says that he had a “sore” on the outer surface of the left 
stump about 1 year ago. He had no pain in the stump until 1 year ago, when a painful 
wound developed that took 3 months to heal. Three months ago pain in the right stumpi 
set in; at the tip a sore developed which refused to heal, and became gradually worse. 

Physical examination, Dec. 15, 1909: This reveals swelling of the entire right stump. 
Posteriorly in the flhp there is an ulcer the size of a dollar with gangrenous margin. The 
whole stump up to the upper border of the patella is discolored; has a purplish reddish hue. 
In the elevated position there is a fair amount of ischemia. The left stump shows marked 
erythromelia, otherwise negative. Both femorals and popliteals fail to pulsate. 

On December 17, 1909, the patient stated that he had had trouble with his right hand 
for several months. He has noticed “swellings” along the front and inner aspects of the 
arm, forearm and hand. The use of his hand has become impaired, the hand has become 
thinner, and the skin relatively thicker and dryer. 

On physical examination of the right hand it is seen that all the fingers look like those of 
sclerodactyly; movement of the distal joints is diminished. The skin is atrophic, dry, and 
the circumference of each finger is considerably less than that of the fingers of the left hand. 


THROMBO-ANGIITIS OBLITERANS—PATHOLOGY IN LETHAL CASES 373 


No radial or brachial pulse is palpable; the brachial artery can be felt as a hard cord. An 
axillary pulse can be obtained. 

Examination of the vessels of the left hand reveals absent radial and ulnar pulsations, 
fairly good brachial pulse. There are no trophic disturbances. 

Neither femoral pulse is obtainable. 

X-ray examination of the hands, Dec. 23, 1909, shows atrophy of all the hones. 

The patient was readmitted to the hospital April n, 1911, complaining of pain in the 
left stump; the condition of the hands unimproved. 

April 26, reamputation of the left stump for ulceration and sloughing. The femoral 
artery and vein were found occluded. May 2, skin flaps blue and poorly nourished; 
May 5, no union of external half of wound, union of inner half incomplete, tissues appear 
necrotic. May 25, during the past few days the patient has become more lethargic; 
temperature ranges from 100 to 102.5 0 ; tongue dry, cracked; patient unable to answer 
questions, drowsy; left stump necrotic; May 30, patient considerably weaker and comatose, 
exitus. 

Autopsy Diagnosis: Thromho-angiitis Obliterans , Thrombosis of Abdominal Aorta .— 
General—body is that of a rather emaciated man, marked rigor mortis, both lower limbs 
amputated through the thighs. 

Heart—rather smaller than normal; subpericardial fat slightly increased in amount. 
Tricuspid valve admits 4 fingers, and tricuspid flaps are normal. Right ventricle is widely 
dilated; muscle quite brownish and extremely thin. Some invasion of the muscle by sub¬ 
pericardial fat. Pulmonary valve shows no abnormality; no signs of atherosclerosis in the 
pulmonary artery; left ventricle endocardium somewhat whitened. Mitral orifice admits 
3 fingers easily; mitral flaps very slightly thickened; left ventricular muscle brown and of 
about normal thickness; avenue of outflow widely thickened. Aortic valve shows slight 
fenestration and thickening of the corpora Arantii, corresponding to about the third 
degree of atherosclerotic process. 

The aorta elasticity is normal; a few, small, fatty areas in the intima around the orifice 
of the anterior coronary artery; a few very slight fatty plaques in the intima of both 
coronaries. 

Aorta—from the arch down to the level of the superior mesenteric is of normal thickness 
and elasticity, and shows only a very few, small, yellow, fatty areas in the intima. The 
vertebral branches come off regularly. The coeliac axis and its branches show not the 
slightest thickening, similarly with the superior mesenteric, but beginning just below 
the origin of the latter, is a fusiform expansion of the aorta about 3 cm. long, 2.5 cm. wide 
and 2 cm. thick. Below this the nature of its continuation is doubtful because the aorta 
has been torn off just above the bifurcation, but, although the swelling tapers downward, 
it probably was continued into the iliacs. 

Around the swelling of the aorta is dense fibrous tissue (periarteritis). On cutting 
through the center of the fusiform swelling the aorta is found to be filled with a mass of 
what appears to be organizing thrombus. The vessel wall itself appears even thinner than 
normally. The mass of tissue in the lumen is firmly adherent to the wall of the vessel. 
The part on the periphery of the mass and immediately adjacent to the intima is firm and 
yellowish in color, whereas the central part is of a cherry red color and much softer. Just 
to one side of the center the material is a deep red, very soft and resembles more closely 
rather fresh clot. When the aorta is opened down to the beginning of this process and 
when the mass within the lumen is viewed from above downward it is seen to bdgin 0.5 
cm. below the origin of the superior mesenteric artery, here being entirely parietal and 
adherent to the intima of the anterior half of the vessel wall. The vessel is completely 
closed about 2 cm. below the origin of the superior mesenteric artery, but as has just been 
said, it sends up a parietal tongue-like process which is adherent to the anterior half of the 
wall. This tongue-like process is of a deep pink color, firm in consistency and densely 
adherent to the vessel. The two renal arteries are given off above the level where the 
aorta is completely occluded, and from the portion of the aorta which contains the 
parietal mass. The left renal appears normal and is perfectly free of clot, but the right 
renal contains at least for 7 mm. from the point of origin (which is all the vessel that is on 
the specimen), a parietal mass which is firm in consistency, pinkisft grey in color, semi- 
translucent. It is about 1 mm. in thickness, and runs completely around the entire cir¬ 
cumference of the vessel, narrowing the lumen to a diameter of 2 mm. 

Liver, pancreas and intestines negative. 

Right kidney—shows evidence of parenchymatous degeneration, striations poorly 
marked. Renal artery and vein show no changes whatever. 

Left kidney—cortex about normal thickness and the markings extremely faint; 
peripelvic fat increased in amount. Near the upper pole of the organ and situated about 0.5 
cm. beneath the surface is a multilocular cavity containing greenish pus, the walls of which 
are smooth and consist of fibrous tissue, in some places being 2 mm. thick. 


374 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Microscopic Examination. —This showed none of the typical lesions of 
thrombo-angiitis obliterans in the aorta or renal vessels. The lesions were 
those of recent thrombosis with bland type of organization and arteriosclerosis. 


CHAPTER LXIV 

THROMBO -ANGIITIS OBLITERANS—DIAGNOSIS 

Much to the confusion of our diagnostic concepts of the circulatory 
affections, individual and combinations of manifestations loom up and enter 
into the clinical field under extremely varied disguises. 

Thus, pain on walking may be associated with blanching of the feet; or, 
spontaneous vasomotor ischemia may be followed by rubor and cyanosis— 
both types occurring in thrombo-angiitis obliterans, and ^mimicking 
Raynaud’s disease. 

Chronic rubor and pain, a combination common in thrombo-angiitis 
obliterans and atherosclerotic vascular occlusion may simulate erythrome- 
lalgia. 

The chronic atrophies and the indurated skin sometimes accompanying 
advanced lesions of thrombo-angiitis obliterans may be mistaken for 
scleroderma and sclerodactyly. 

The transmutations and kaleidoscopic nature of the dominant features 
of thrombo-angiitis are in singular contrast with the more stable clinical 
symptoms of the vasomotor neuroses. 

Thrombo-angiitis obliterans must be diagnosticated from, first , lesions 
of other organic vascular diseases of the extremities, second , cases of neuro¬ 
pathic or neurogenic vascular disorder of the extremities. In the first group 
belong athero- and arteriosclerotic gangrene, endarteritis obliterans, embolic 
and thrombotic gangrene. In the second group belong Raynaud’s disease, 
erythromelalgia, acro-paresthesia, multiple neurotic gangrene, scleroderma, 
sclerodactyly, and chronic acro-asphyxia. A careful clinical study of 
thrombo-angiitis obliterans will dissipate all doubt as to the possibility of, 
separating this disease, as a clinical entity, from the other types of organic 
vascular disease, as well as from all those neurogenic varieties of vasomotor 
and trophic disorders that may be clinically confounded with it. 

Characteristic for thrombo-angiitis obliterans are the following groups of 
symptoms: (i) the disappearance of the pulses, particularly the dorsalis pedis, 
posterior tibial, and popliteal, more rarely the femoral, radial and ulnar; (2) 
the development of typical manifestations of impaired circulation, to wit: 
Blanching of the lower extremities when these are elevated above the horizon¬ 
tal, hyperemia (rubor or erythromelia) or reddening of the foot in the depen¬ 
dent position during certain stages of the disease, and trophic disturbances, 
such as impaired growth of the toe nails, slightly atrophic condition of the 
skin, ulcers, and gangrene; (3) true vasomotor phenomena of transitory 
nature, such as alternating syncope, rubor, coldness apparently independent 
of those chronic changes that have been cited above, and that are distinctly 
traceable to the occluded condition of the arteries and veins; (4) the 
symptoms of pain, either in the form of intermittent claudication (pain in the 
calf of the leg or in the foot on walking with cessation when the limb is at 



TH ROM BO-A NGIITIS OBLITERA NS—DIAGNOSIS 


375 


rest) or the severe pain that is associated with the advent of trophic distur¬ 
bances, especially with ulcers and patches of gangrene; (5) the slow course of 
the disease, symptoms of intermittent claudication or pain, preceding the 
development of trophic disturbances for months and years; (6) the fact that 
about 99 per cent of the cases occur in Polish, Galician or Russian Hebrews, 
and that almost always young males between the ages of twenty and thirty 
are taken with this disease; (7) the onset of symptoms in the lower extremi¬ 
ties, one of the legs being first affected; (8) the comparative infrequency of 
involvement of the upper extremities; (9) the association of a peculiar type of 
migrating phlebitis in the territory of the external or internal saphenous, less 
frequently in the larger veins of the upper extremities, characteristic in about 
20 per cent of the cases; (10) the slow but steadily progressive course, leading 
in a large majority of the cases to amputation of at least one limb, not infre¬ 
quently of both lower extremities, and in rarer instances to amputation of one 
of the upper extremities as well. 

For the clinical diagnosis of thrombo-angiitis we must depend upon (1) 
the racial (Hebrew) and sex (male) predilection; (2) the early involvement of 
the lower extremities; (3) the early symptoms of pain or intermittent claudi¬ 
cation; (4) the presence of migrating phlebitis; (5) the evidence of pulseless 
vessels; (6) the presence of blanching of the extremity in the elevated position; 
(7) the existence of rubor in the dependent position; (8) the relation of the 
hyperemic phenomena to posture; (9) the absence of simultaneous, symmetrical 
involvement; and (10) the slow, progressive chronic course terminating in 
gangrene. 

Differential diagnosis between thrombo-angiitis obliterans and the vaso¬ 
motor neuroses: Were it not for the fact that certain symptoms, closely 
resembling typical vasomotor phenomena, may persist for weeks and years in 
this disease, confusion with the true neurogenic vasomotor process would 
scarcely ever arise. The chronic condition of redness in thrombo-angiitis 
obliterans can be explained as due to dilatation of the superficial capillaries, 
this being a compensatory phenomenon making for an adjustment of the 
impaired circulation. This chronic redness or rubor may be mistaken for 
erythromelalgia, or for the rubor of Raynaud’s disease. The fact that it is 
associated with other evidences of closed vessels and the other characteristic 
features above mentioned, together with the circumstance that the redness 
disappears at once upon elevating the extremity, will make the recognition 
of its nature possible. 

For the recognition of thrombo-angiitis of the upper extremities, it is well 
to separate the cases in which vasomotor symptoms predominate, from 
those in which the symptoms in the lower extremities are well marked; and 
also, to distinguish those in which we are compelled to investigate very care¬ 
fully in order to elicit evidences of vascular occlusion. 

The symptoms simulating Raynaud’s disease and acro-asphyxia are cyan¬ 
osis of the finger tips, coldness of the fingers with or without trophic distur¬ 
bances, and alternating cyanosis and rubor, involving the fingers or the whole 
hand. Rather characteristic in the symptomatology of thrombo-angiitis is 
the apparent dependency of the vasomotor symptoms upon variations in 
temperature, the chronicity of the manifestations, the absence of pain in some 
of the cases, and the absence of paroxysmal nature of the attacks so character¬ 
istic in Raynaud’s disease. 

When we turn to those patients in whom the trophic disturbances seem to 
be unassociated with evidence of vasoconstriction and vasodilatation we note 
that there is merely a history of the development of a spontaneous ulcer of the 


376 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

fingers. It seems more than likely that in many of these the history of the 
absence of the vasomotor phenomena would be found unreliable if it were 
possible to observe the cases throughout the whole course of the disease. 
Future observations will probably support my belief that here, too, some mani¬ 
festations of deranged vasomotility do occur. 

When we consider the largest group, namely, that in which gangrene of 
small or greater extent develops, we find that some cases may be mistaken for 
simple paronychia. Others claim that the development of a gangrenous 
patch or of the felon was preceded for a long time by distressing pains in the 
tips of one or more fingers. The vasomotor symptoms may be absent or the 
cyanosis and redness may be quite striking. The following sequence of 
symptoms may be observed and is interesting, because pain and trophic 
disturbances alone are complained of. The onset is marked by severe pain 
in the tip of a finger. This is superseded by atrophic changes in the skin, 
the development of a dry, hard patch, mortification, and also formation of an 
ulcer. In still other cases the similarity with Raynaud’s disease is even more 
marked, for the symptoms are pain, cyanosis, rapidly followed by gangrene. 

More rarely do we meet with those interesting examples of the effects of 
arterial occlusion in which the development of intense atrophy of a hand or 
limb or the production of the typical picture of scleroderma and sclerodactyly 
is the significant feature of the clinical picture. 

The differential diagnosis of this condition from the vasomotor neuroses 
may however be difficult in the cases in which we cannot exclude the associa¬ 
tion of the 1 two diseases. It will be noted that where coldness and cyanosis 
are complained of, a distinct dependency on temperature or other environ¬ 
mental condition can often be elicited or that pain is absent. The presence 
of vessel changes and the history of the involvement of a lower extemity at 
once clear up the diagnosis. 

Where trophic changes alone are present, the absence of symptoms refer¬ 
able to the central nervous system speaks decidedly against nerve lesions. 
The relation of the vasomotor symptoms to the position of the limb will in 
other cases be of value in explaining the nature of the symptoms. 

How can we explain the occurrence of true vasomotor phenomena such as 
do not seem to owe their existence to the mechanical effects of impaired 
circulation? The blanched appearance that is a sequence of an obstructive 
condition of the arteries, and which can be demonstrated by elevation of the 
leg, and in bad cases can even be elicited in the horizontal position, is a phe¬ 
nomenon easily explicable on the theory that the avenues of arterial supply 
are cut off through extensive obturation of the arteries. Many clinical and 
experimental observations have been gathered that speak in favor of this 
view.. So also is the rubor not a true vasomotor phenomenon, but a sign of 
chronic vasodilatation of the superficial capillaries and is compensatory in 
nature. The part played by the vasomotor mechanism in its production is 
discussed in Chap. XLVI. 

On the other hand, veritable symptoms of disturbed vasomotility can be 
associated with thrombo-angiitis obliterans . That these should occur is 
not surprising when we call to mind that not only have intense and extensive 
destructive, pathological alterations taken place in the most important arteries 
of a limb, but that the accompanying nerves are frequently bound down by 
a dense mass of cicatricial tissue and have undergone severe fibrotic changes. 
Although the mechanism of the irritative and exhaustive vasomotor 
phenomena is not clear, the total disorganization of the vascular innervation 
in many of the cases would seem to afford some basis for the possibility of the 


TH ROM BO-A NGIITIS OB LI TERA NS—DIA G NO SIS 


377 


occurrence of the disturbances which we call “vasomotor” in nature 
Other theories are discussed elsewhere. 1 

Where signs of thrombo-angiitis of the lower extremities are unquestion¬ 
ably present, and where evidences of vascular occlusion in the upper extremi¬ 
ties are lacking, although these are the site of disturbed vasomotor innervation 
we may for a long time be unable to rule out the possibility of the 
simultaneous occurrence of two different diseases. 

In addition to this more or less chronic or permanent sign of deranged 
circulatory function in thrombo-angiitis other phenomena which are truly 
vasomotor in nature may frequently be associated; and, it is these that must 
be differentiated from similar phenomena accompanying Raynaud’s disease, 
erythromelalgia, scleroderma, sclerodacytly, and acrocyanosis. 

In order that a differential diagnosis may be clearly presented, 
let us briefly recapitulate the typical course of a case of Raynaud’s disease! 
The latter is an affection whose pathology has not as yet been definitely deter¬ 
mined, the lesion doubtlessly . residing somewhere in the central nervous 
system. Its clinical characteristics may thus be summed up: Somewhere in 
the peripheral portions of the body (so-called acra) there occurs more or less 
severe pain not confined to distinct nerve territory, usually affecting sym¬ 
metrical parts, attacks of vasomotor disturbance being part of the syndrome. 
These latter are (i) syncope, asphyxia, or local rubor, and (2) severe trophic 
disturbances, usually in the form of gangrene of the parts first affected with 
symptoms. The course is. an intermittent one, for there may be completely 
free intervals; but in some instances, evidences of disturbed vasomotility may 
persist. The disease may consume itself in one attack or several attacks may 
occur in succession. Objectively, sensory disturbances are usually absent, 
as well as paralysis, although other evidences of disturbed vasomotor inner¬ 
vation, such as aphasia, hemoglobinuria, arthropathy, may occur. Usually 
neuropathic individuals are affected. The organic vascular changes, as well 
as the lesions of the nervous system, reported as occurring in some of the 
cases, have doubtless no causative relation with the disease. 

It is true that there are still some who cling tenaciously to the theory that 
some lesions of the peripheral arteries may account for the symptoms of Ray¬ 
naud’s. disease. In support of this view, certain anatomical findings have 
been cited as strong arguments by those who believe that a definite 
anatomical lesion in the peripheral vessels is irresistible testimony 
against pure hypothesis. A careful analysis of the cases in question, as made 
by Cassirer , shows that reported organic alterations in the vessels will 
not suffice to explain the symptoms any more satisfactorily than the theory of 
a central nerve affection of the sympathetic system. Whereas in thrombo¬ 
angiitis, obliterans the territory manifesting symptoms, corresponds to that 
containing the diseased vessels, we find that no such relation exists where 
vascular lesions are associated with Raynaud’s disease. 

In Raynaud’s disease we will note the following features: A sudden onset 
of the first stage of local syncope or regionary ischemia involving usually the 
fingers, more rarely the toes, and occasionally the margins of the ears or the 
tip of the nose with coldness and blanching; associated sensory phenomena, 
paresthesia, and pain; a comparatively short duration of the vasomotor and 
sensory manifestations, their intermittent character with return to normal 
between the attacks; the symptoms of local asphyxia attended with local 
depression of temperature and swelling of the parts involved; the disappearance 

1 Chap. LXXXVI, also Chap. LIV. 


378 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


of the asphyxia with substitution of reactive hyperemia and a third stage of 
dry gangrene. Characteristic for this disease as well as for the cases of sclero¬ 
derma and sclerodactyly is the striking atrophy of the ends of the distal 
phalanges. The changes in the bones can be well demonstrated by Roentgen- 
ray examination, atrophy and disappearance of large portions of the end- 
phalanges being distinctive and diagnostic features. In our own experience 
the alterations in the bones could be detected early in the disease, probably 
developing simultaneously with the other trophic disturbances. 

The differentiation of true scleroderma from thrombo-angiitis will be rarely 
difficult to make. In scleroderma and sclerodactyly the first stage with hard 
edema is characteristic and never simulated by cases of organic vascular 
disease. The second indurative stage may, however, be almost exactly repro¬ 
duced by other affections. The form of scleroderma known as “ sclerodactyly ” 
because of attendant alterations in the deeper tissues, may not be unlike 
thrombo-angiitis. Roentgen-ray examination of the hand in sclerodactyly 
offers the most valuable means of differentiating the two diseases. The 
phalanges will very early show atrophic changes and disappearance 
of the terminal portions in scleroderma, sclerodactyly, and Raynaud’s 
disease, while the bones, although somewhat rarefied, will be seen to conserve 
their outlines throughout the course of the disease, thrombo-angiitis obliterans, 
until they are disturbed by the effects of gangrene. 

So far as our experience permits us to judge, symptoms of scleroderma 
occur only late in thrombo-angiitis when other signs of vascular occlusion have 
already become well developed. The recognition of the condition will then 
depend upon the absence of pulsation in the larger peripheral vessels, the 
presence of gangrene (or the history of such a condition) and of the other typical 
signs of obliterated arteries and veins. 

It is most probable that in Raynaud’s disease and the related affections the 
seat of the pathological process is to be sought in the vegetative system, that 
is, somewhere in the vasomotor apparatus. Nor are we likely to be rewarded 
in a search for any organic change. The frequent return to a normal con¬ 
dition, observed clinically, also speaks against the likelihood of morphological 
or chemical alterations in the nervous system. 

Whereas in thrombo-angiitis obliterans a definite and specific morpho¬ 
logical change in the arteries and veins is responsible for the varied phenomena 
in the superficial capillaries, in Raynaud’s and allied diseases, the vasomotor 
and trophic disturbances are the outcome of irritative and exhaustive proc¬ 
esses of the sympathetic nervous system. 


CHAPTER LXV 

THROMBO -ANGIITIS OBLITERANS—TREATMENT 

It must be remembered that we have as yet no treatment for the acute 
stage of the disease in the sense of a procedure that has specific effect on the 
acute inflammatory process in the arterial and venous walls. Nor have we 
any prophylaxis against the disease. Whether salvarsan injections or drugs 
of similar action or other bactericidal agents may be of value, we cannot as 
yet determine, in view of a too limited experience. Certain it is, that when 



THROMBO-ANGIITIS OBLITERANS— TREATMENT 


379 


we speak of treatment of the disease, we are in truth referring to therapeusis 
of the consequences of the “healed stage” and not of the morbid process per 
se. With this qualification, therefore, we may proceed to the discussion of 
what is known regarding the care of the many effects of the resultant 
impaired circulation. 

The treatment should vary according to the stage of the disease, the 
presence of migrating phlebitis, trophic disorders and gangrene. Since the 
methods recommended for atherosclerotic cases often apply here, it is well to 
read the two chapters in this connection. 


PROPHYLACTIC TREATMENT 

If we accept the theory that the process is one induced by some infectious 
agent in arteries that exhibit a certain predisposition to disease, it is quite 
evident along what avenues future investigations of preventitive nature 
should be directed. In all susceptible individuals then (racial proclivity, 
etc.) both the predisposing forces and the inroads of the specific type of 
noxious agent are subjects of concern. 

To combat the former, all the usual stresses of mechanical or chemical 
nature that produce arterial inferiority (excessive exercise, exposure, certain 
foods, tobacco, etc.) must be avoided. As for the latter, however, we are 
still at a loss for either a preventitive serum or medicament. 

It would not be paradoxical to state that the only efficacious treatment 
of this disease is one of pure prophylaxis. For even with the most careful 
scrutiny and search for evidences of arterial involvement, we are usually 
unable to recognize the existence of the disease before arteries and veins 
over considerable territory are already irremediably damaged. It is per¬ 
haps only in those cases where a period of migrating phlebitis ushers in the 
malady and precedes the involvement of the deep vessels by months or years, 
that there is given us a period during which experimental work of preventi¬ 
tive therapeutic nature can be applied. 

As soon as signs of obstructive vascular lesions are diagnosticated, even 
before the advent of destructive alterations in the peripheral tissues, great 
stress should be laid on the importance of diminishing the functional demands 
on the local circulation. The agencies that are likely to disturb the fine 
balance between the tissue requirements and the permanently defective 
circulation, are the following: Prolonged standing, walking, compressing 
forces that produce local anemia, such as tight shoes, bands, etc.; exposure 
to cold with its sequence—ischemia of the parts (or to cold and moisture); 
mechanical insults that produce clean wounds or infections and thus call 
forth the need of an enhanced circulatory activity. In short, the locomotor 
apparatus must be spared as much as possible for its adaptive or accommo¬ 
dative powers are greatly reduced in this condition. 

Treatment of Pain.—Clinical experiments have been carried mit by the 
author and others with a view to blocking the afferent nerve paths. The 
Foerster posterior root section 1 has not found aceptance because of the 
magnitude of the operation. Silbert 2 recently reports complete relief of 
pain in 3 cases after the injection of absolute alcohol, care being exercised 
not to infiltrate adjacent tissues. Anesthesia of the sole of the foot with 
relief of pain is said to result immediately. Because of the occurrence of 

1 Elsberg, Case observed by author. 

2 Silbert, Jour. Am. Med. Assn., Nov. 18, 1922, 79, 1765 


380 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


late palsies and trophic ulcerations the author does not recommend this 
method. 


II* CONSERVATIVE TREATMENT 

When the disease is well developed, distinct intermittent claudication being 
present and fairly marked pain with or without trophic disorders, it is 
advisable that the patient remain in bed for several weeks or even longer, or 
at least that walking and standing be completely interdicted. Therapeutic 
measures should be directed towards the conservation of warmth, enchance¬ 
ment of the circulation, the prevention of traumatism, and the treatment of 
local conditions, trophic disorders or gangrene, when these supervene. 

A. Methods of Enhancing the Circulation, i. The Postural Method .— 
The author has suggested that certain passive exercises may be of value in 
inducing hyperemia or rubor in the affected limb, and therefore, thera¬ 
peutically beneficial in increasing the blood supply. 

This method is the logical therapeutic outcome of the author’s method of 
diagnosticating impairment of circulation of the lower extermities, in that it 
uses the phenomenon of induced rubor , or induced hyperemia in a therapeutic 
way. If the method be carried out daily for a sufficiently long period, it 
is of greater value in improving the circulatory conditions and in increasing 
the blood supply, than any of the other mechanical or thermal means that are 
at our disposal. 

The procedure is as follows: The affected limb is elevated with the patient 
lying in bed, to from 6o° or 90° above the horizontal, being allowed to rest 
upon a support for from 30 seconds to 3 minutes, the period of time being the 
minimum amount of time necessary to produce blanching or ischemia. As soon 
as blanching is established, the patient allows the foot to hang down over the 
edge of the bed for from 2 to 5 minutes, until reactionary hyperemia or rubor 
sets in, the total period of time being about 1 minute longer than that necessary 
to establish a good red color. The limb is then placed in the horizontal 
position for about 3 to 5 minutes, during which time an electric heating pad 
or a hot water bag is applied, care being taken to prevent the occurrence of a 
burn. The placing of the limb in these three successive positions constitutes 
a cycle, the duration of which is usually from 6 to 10 minutes. These cycles 
are repeated over a period of about one hour, some 6 to 7 cycles constituting 
a seance. 

The number of seances cannot be categorically stated but should vary 
with the case. In a general way they should occupy at least 6 to 7 hours a 
day, that is every alternate hour during the daytime. During the hours of 
rest, heat is applied continuously in the form of an electric pad, hot water 
bag, hot air apparatus, or electric lamp. 

In the opinion of the author, this method does far more to improve the 
circulation than either the application of superheated air (so-called baking 
treatment), or the diathermic treatment. 

The length of time of its application may require modification according 
to the manner in which the procedure is borne. In some cases pain induced 
by elevation may necessitate a diminution in the period of elevation. 

It is not possible to lay down hard and fast rules as to the exact application 
of this method in any given case. Its employment should be varied accord¬ 
ing to the requirement of each and every clinical stage, and the patient’s 
response. A more detailed discussion will be found in the chapter on Arterio¬ 
sclerotic Gangrene. 


THROMBO-ANGIITIS OBLITERANS— TREATMENT 


381 


2. Heat .—For the cases of thrombo-angiitis obliterans, as well as arterio¬ 
sclerosis, it is best to exclude the foot from the hot air treatment, when it is 
the seat of trophic disorders or gangrene. Heat may be applied either by 
means of an electric thermophore, by a hot-air apparatus, or an incandescent 
apparatus containing one or more incandescent lamps, or a single strong 
electric lamp with reflector. The temperature should not be raised higher 
than i2o° F. at the first treatment, and gradually increased to 150° and 180°, 
but never more than 200° F. Heat is applied as high as the middle of 
the thigh, for about one-half hour. In the presence of migrating phlebitis 
this treatment is not well borne. Whenever gangrene is present, the 
gangrenous part is left covered with a dressing but not included in the 
apparatus. 

The frequency of the heat treatments is to be varied in accordance with 
the reaction and the exact condition of the affected limb. It cannot be 
emphasized too strongly, however, that occasional applications (once or 
even twice in 24 hours) are of little therapeutic value, and that treatment over 
prolonged periods of time is necessary to obtain beneficial results. 

3. Diathermic Treatment .—This is an excellent method of obtaining the 
effects of heat upon the deeper parts, and is particularly applicable to the 
early cases, especially those in which intermittent claudication is the most 
marked symptom, and in those patients in whom ambulatory treatment must 
be carried out. In the presence of inflammation, migrating phlebitis, ulcers 
or gangrene, it does not seem to be well borne or beneficial. The seances 
should last from twenty to twenty-five minutes. 

The patient will feel the development of the heat in the region of the 
ankle, where the effects of warmth can be demonstrated by the touch. 
Subjectivelv, there is in addition to the feeling of heat, a dull ache which 
should not be allowed to become marked. Pain is a sign for diminishing the 
strength of the current. 

Some authors claim success in the treatment of thrombo-angiitis oblite¬ 
rans by the diathermic method, which H. Wolf employs as follows. 

The patient sits on a chair with each foot in a basin of warm salt water. 
Each basin is connected with one of the poles of the diathermic apparatus. 
This can be done simply by putting an electrical plate electrode with con¬ 
necting wires into the water. The current is then turned on and increased 
according to the sensation of the patient, usually to about 7 00 M.A. The 
patient is allowed to increase and decrease the amount of current at will, so 
as to avoid excessive current strength. If it is desired to concentrate the 
current in the toes, a block of wood is placed under the heel so that it stands 
above the water. The current is then forced through the toes mainly, and 
the effect is stronger. The duration of treatment is from 25 to 30 minutes. 
The frequency depends upon the reaction. With the occurrence of inflamma¬ 
tion or phlebitis, the treatment is discontinued. After subsidence of such 
complications, the treatment may be resumed and given daily. 

4. Many attempts have been made to improve the circulation through the 
subcutaneous or intravenous injection of solutions that might diminish the 
viscosity of the blood. So Koga 1 employed Ringer’s solution. Ginsberg 2 
and Steel 3 have suggested sodium citrate intravenously. Others (Meyer 4 ) 
have claimed beneficial results after flushing the intestinal tract daily with 

1 Koga, Deut. Zeitschr. f. Chir., 1913, p. 371- 

2 Ginsberg, Am. Jour. Med. Sc., (Sept.), 1917, 154, 3 2 °* 

3 Steel, Jour. Am. Med. Assn. (Feb. 12), 1921, 76, 429- 

4 Meyer, Jour. Am. Med. Assn. (Oct. 19), 1918, 1268. 


382 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


8 to io quarts of Ringer’s solution through a duodenal tube, this supple¬ 
mented by several daily subcutaneous injections of this solution. The 
belief that beneficial results follow intravenous administration of sodium 
citrate solution seems hardly warranted. 

5. Intermittent Compression of the Main Arteries .—An exceedingly tedious 
but sometimes valuable method of inducing reactionary rubor and further¬ 
ing the development of collateral circulation is intermittent compression or 
digital obliteration of the brachial or femoral arteries, when these are patent. 
The circulation in these vessels is made to cease by pressure of one or more 
fingers; the brachial artery being easily accessible at its beginning, the femoral 
just below Poupart’s ligament. Where the facilities are at hand, the artery 
may be controlled for one minute and the circulation allowed to return for 
five minutes, this being repeated over a period of an hour. Such seances 
should alternate with those of the postural method and hot air treatment. 1 

B. Internal Medication.—Mercury may be given in some cases in smaller 
injections when syphilis is suspected, although it does not seem to have any 
material effect upon the disease. Nitro-glycerin and iodides may be adminis¬ 
tered under certain circumstances, although their effects are of questionable 
value. 

C. Local Treatment.—Trophic ulcers must be treated on general surgical 
principles, the combatting of the severe pain attending these being the most 
difficult part of the treatment. An ointment containing 5 per cent novocain, 
and 10 per cent orthoform or anesthesin in lanolin and glycerin is sometimes 
beneficial in allaying local pain due to trophic disorders. The continuous 
saline bath or repeated baths alternating with the postural exercises is a 
valuable adjuvant in aiding healing. 


III. OPERATIVE TREATMENT 

Ligation of the Femoral Vein.—Lilienthal has suggested the ligation of the femoral vein 
as of some value in enhancing the circulation. He claims that in some cases of sudden 
gangrene healing may take place after conservative treatment, such as removal of a toe 
alone, and that frequently a lower amputation will be more apt to be successful after 
ligation of a vein. The author cannot subscribe to this view. 

Arteriovenous Anastomosis.—This has been suggested by Wieting 
with a view to reversing the circulation, the femoral artery and femoral vein 
being anastomosed in such a manner that the vein will receive the arterial 
blood. Wieting and others have reported successful results, cures of impend¬ 
ing gangrene and restoration of circulation. Experimental work, however, 
(Stetten) would tend to show that it is practically impossible to transform 
the veins into arteries by anastomosis, and clinical reports do not justify 
us in recommending this method either is the presence of gangrene, or in 
threatened gangrene. Involvement of the veins in thrombo-angiitis 
obliterans, both superficial and deep, with obliteration in a larger percentage 
of the cases, makes it unlikely that improvement of circulation could occur 
by deflecting the arterial current into the veins. 

1 It is interesting to note that an apparatus for mechanically producing intermittent 
Bier’s venous hyperemia was used in Germany during the Great War, in order to combat 
infection in limbs infected with the gas bacillus. The compressing cuff is distended by 
pressure from an oxygen tank, and a mechanical timing interrupter breaks and makes the 
flow of gas, causing the dilatation of the cuff. It is possible to employ a similar apparatus 
for the intermittent and isolated compression of single large arteries. A small electric 
motor may furnish the power for air pressure, and a pneumatic cushion may be so adjusted 
as to compress the femoral artery. 


TH ROM BO-A NGIITIS OB LI TER A NS— TREA TM ENT 


383 


Not only theoretic consideration but also practical experience have been 
convincing in demonstrating the futility of attempting arteriovenous anasto¬ 
mosis in this disease. Thus we may cite the following instructive instance of: 

Functional failure of arteriovenous anastomosis; bone formation in , and 
occlusion of anastomosed area. 

Case L. W., age 32, Russian Hebrew, June 15, 1913, says that he has been troubled for 
two years with pain in the right leg. He had had an arteriovenous anastomosis done at the 
Beth Israel Hospital on November 5, 1912, but he did not feel improved by the operation. 
On physical examination, June 20, 1913, the right foot was considerably enlarged by 
reason of edema, cyanotic, very painful, showed some atrophy, marked ischemia in the 
elevated position. 

On June 23 the patient begged for amputation because of the pain. The author 
decided to expose the site of the anastomosis both for purposes of discovering what had 
occurred and possibly whether another anastomosis was feasible. A considerable amount 
of scar tissue was found about the situation of the vessels. The artery and vein were 
embedded in a mass of connective tissue. They were liberated with some difficulty and a 
piece of artery and vein, three inches in length, was excised. Both the artery and vein for a 
distance of five inches were found converted into hard pipe stem-like cords. 

Histological examination showed complete obliteration of the vessel by connective tissue 
and bone formation. 

When this condition was found at operation, it was decided to proceed with amputation. 
A Gritti-Stokes was done with an excellent result. 


In view of the bad outlook in these cases, it is not to be wondered at, that 
even peri-arterial sympathectomy of the larger arteries (femoral) should 
have been suggested and tried. The author has elsewhere called attention 
to the fact that little can be expected from such an operation on a priori 
grounds. 

Strauss 1 reports decortication of the right femoral artery for a distance of 8 cm. in a case 
of thrombo-angiitis obliterans. Although the pain is said to have been influenced for a 
short time, gangrene soon supervened and pain returned. From the experience in this and 
another case, this author concludes that the consequent vasodilatation is only transitory, 
and that the beneficial results are only temporary. 


Limited Amputation.—Amputation of a toe alone is often unsuccessful 
for healing may not take place. In some instances, however, conservative 
treatment such as described above, together with ablation of a toe alone, or 
several toes if necessary, may be followed by good results. In the majority 
of cases amputation at a point higher up will be necessary. 

Radical Amputation.—In the majority of cases amputation of at least 
a portion of the leg will become necessary. The Gritti-Stokes amputation 
is the ideal procedure in these cases, although lower amputations are occasion¬ 
ally successful. The author found that in a series of 65 amputations accord¬ 
ing to the Gritti-Stokes method primary union was obtained in all instances. 2 
When amputation is performed lower down, healing may take place, but in 
many instances sloughing of the flaps occurs, and secondary amputation 
becomes necessary. Inasmuch as the disease occurs for the most part in poor 
working people, it seems that the Gritti-Stokes amputation is preferable to 
those methods which are dubious in their outcome and require many months 
for the accomplishment of their purpose. Methods or tests for estimating 
the point at which amputation should be done are all unreliable. 

Some surgeons would prefer circular amputation through the lower part 
of the thigh, if, in their experience a better artificial knee joint can be thus 
applied. The author has had eminently satisfactory results with the Gritti- 


1 Strauss, Surg., Gynec. & Obst., Feb., i 9 2 3 > 3^, p- 290. , 

2 In one case the patient died of pulmonary embolism about eight days after 


the 


operation. 


384 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Stokes amputation. Whenever complicating ascending lymphangitis or 
severe infection is present, the amputation must be done much higher 
through the thigh. 

THE SELECTION OF THERAPEUTIC PROCEDURES 

Here, as in the arteriosclerotic cases, careful attention to details and 
proper clinical inferential reasoning will help us select a combination of 
methods that may ward off gangrene or even give considerable comfort to 
the patient. 

The cases with minimal symptoms, coldness of the toes or foot, possibly 
intermittent claudication, with or without spontaneous pain, are those that 
should receive special consideration. For, with intensive prophylaxis, correct 
appreciation of the gravity of a seemingly minor affection, the patient’s 
limbs may be preserved for many years and their utility prolonged or made 
permanent. It is advisable to recommend, in such cases, a preliminary 
“cure” or treatment in which absolute rest in bed is required for at least 4 to 
6 weeks. During no part of this time is the patient allowed to walk, although 
after the first 2 weeks it is well to permit the shoes to be put on for 3^ hour a 
day, provided the latter do not constrict or hurt in any way. Smoking is 
prohibited. Injections of sodium iodide are given intravenously, and if we 
wish, flushing of the alimentary canal with Ringer’s or Locke’s solution 
through a duodenal tube may be given a trial. This method has been 
recommended (W. Meyer) to decrease the viscosity of the blood. 

The greater part of the day is occupied with the manipulations for enhanc¬ 
ing the circulation, namely, the postural and hot air methods. The former 
should occupy every other hour of a 16 hour day, excluding an hour’s rest for 
lunch and dinner and should alternate with similar periods of hot air treatment 
(about 40 minutes each). Restriction of one or the other may be found 
necessary by virtue of special reactions of the patient. 

After the 4 to 6 weeks, the postural and hot air seances are to be continued 
for about 6 hours a day (each 3 hours), the distribution of application being 
adjusted so as to suit the patient’s habits. As improvement occurs, reduction 
in the daily duration of treatments is in order, a more intensive resumption of 
the same being indicated upon the slightest recurrence of symptoms. 

When the patient is willing and able to cooperate, intermittent com¬ 
pression of the femoral artery for 30 seconds every 5 minutes over hourly 
periods, may effect the same reaction as the postural treatment, and enhance 
the circulation. 

When migrating phlebitis is present, we must distinguish between the mild 
and the severe cases. Whilst in the former, the postural and hot air treat¬ 
ments may find no absolute contraindication if carefully carried out and in 
reduced measure, absolute rest alone with wet dressings and warmth are the 
best means of alleviating the symptoms in the more severe cases; 

In the more advanced cases with trophic lesions, we must treat the circu¬ 
lation and the local sequelae of disturbed nutrition. Where pain is not 
intensified by the changes of position of the limb, the postural method may be 
carried out as above described. But careful attention must be given to the 
rapidity with which blanching sets in on elevation, lest we unduly prolong the 
time of anemia. So, too, the reactionary rubor may be attended with pain, 
whose advent may require abridgement of the period of pendency. 

Where dry gangrene is present, we combine the postural, hot air, prophy¬ 
lactic measures and intravenous medication. But when ulcers, infection, or 


ATHERO- OR ARTERIOSCLEROTIC DISEASE 


385 


retention of secretions under a nail are observed, the continuous or multiple 
baths of hypertonic salt solution may be invaluable. We should not fail to 
cut away a dead nail that favors retention of secretions in spite of the 
patient’s remonstrance. We must then try out whether permanent baths 
or intermittent baths alternating with 40-60 minutes of postural exercises 
are the best combination in any given case. 1 

Where there are trophic lesions, the intermittent warm baths are so 
valuable as to warrant a trial in every case. The water is kept at 90° to 
98° F., the temperature being varied according to the patient’s ability to 
endure local moist heat. The methods of employing baths that are advo¬ 
cated by the author are the following: The limb is immersed therein during 
the dependent phase of the cycles of postural treatment for half hour or 
hourly periods. Immersions are arranged so as to alternate with the postural 
exercises and banking. 

When conservative methods fail, or there is a fulminating type of gang¬ 
rene, when severe infection complicates, or from the very outset larger 
areas become mortified, amputation will be indicated. 


CHAPTER LXVI 

ATHERO- OR ARTERIOSCLEROTIC DISEASE—CLINICAL 
MANIFESTATIONS 

The clinical picture resulting from intense arteriosclerotic disease of 
the vessels of the extremities, particularly of the lower extremities, is attribut¬ 
able to the effects of impaired or even arrested circulation in arteries whose 
lumina have become narrowed or completely obstructed. By virtue of 
proliferative changes that occur in the walls of the vessels, particularly in 
the intima, and because of the deposition of atheromatous and calcareous 
material, the arterial lumen becomes gradually narrowed, and the normal 
elasticity of the vessel walls becomes lost. In addition to the two factors, 
obstruction by hyperplastic products and loss of normal elasticity, occlusive 
thrombosis may be superadded, these three elements being responsible for the 
circulatory changes in the diseased arteries. 

Although gangrene is the most striking and most severe termination or 
outcome, when the vessels of the lower extremities are afflicted with intense 
and extensive arteriosclerosis, the evolution of this final stage is for the most 
part gradual, the affected limb passing through a number of prodromal stages, 
in which definite evidences of defective circulation can be detected. These 
clinical stages should be recognized and properly appreciated, for, then only can 
the proper prophylactic measures be instituted to delay or even prevent the develop¬ 
ment of the mortifying process. The most important of these clinical pictures 
are briefly the following: 

Clinical Forms of Arteriosclerotic Disease of the Lower Extremities. 

1. Intermittent Claudication. —This symptom may be the only indication of 
arterial disease. Intermittent claudication may be the only manifestation 
of obstructive disease of the arteries, or, it may be associated with absence or 

1 For further details, see Chap. LXXIII, Treatment of Arteriosclerotic Disease of the 
Vessels. 

25 


386 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


pulsation in the dorsalis pedis, or posterior tibial, and popliteal arteries. Later 
on, it is overshadowed by other symptoms. It is not to be regarded as a disease 
per se, but as one of the manifestations of a number of diseases in which the 
arteries of the lower extremities are narrowed or obliterated. 

2. Intermittent Claudication with Other Evidences of Arrested or Impaired 
Arterial Circulation. —Such other phenomena are ischemia on elevation, 
possibly also erythromelia or reactionary erythromelia, attended in some 
instances with coldness and paresthesiae. Vasomotor symptoms are not 
uncommon. 

3. Cases without Trophic Disorders. —Pallor of the foot in the horizontal 
position, or increased pallor on elevation, and moderate or fairly marked hyper¬ 
emia, rubor or erythromelia in the dependent position with absence of pulses, 
may be associated with coldness or occasional cyanosis, in patients who may 
or may not have had symptoms of intermittent claudication. 

4. Cases with Trophic Disorders .—In cases with intermittent claudication , 
ischemia on elevation, rubor, coldness, paresthesiae, absent pulses in certain 
vessels, trophic disturbances in the form of ulcers may develop, slowly or 
suddenly after exposure to cold or some other insult. 

5. Chronic Cases with Inability to Walk. —These may have been preceded 
by intermittent claudication. There gradually develops chronic rubor, 
inability to walk, and pain in the foot. The usual signs of impaired circula¬ 
tion can be elicited. In short, the picture is that of a chronic erythromelia, 
sometimes with edema, without trophic disturbances, but with moderate 
or even intense pain. 

6. Cases with Attacks of Thrombosis. —With any of the above pictures or 
preceded merely by indefinite history of intermittent claudication, sudden 
thrombosis may occur in some of the larger vessels, giving rise to the following 
symptom-complex. The patient will be attacked by sudden pain in the calf 
or in the foot, with inability to walk, and with pallor and coldness of the fore¬ 
part of the foot. On examination, the blanching is seen to be intense upon 
elevation, the dorsalis pedis and posterior tibial arteries may be pulseless, 
whilst the vessels of the other leg are pulsating. After a variable period of 
time, gangrene may set in, or indolent trophic disorders may develop. In 
other cases a condition of chronic rubor may result, with gradual return of 
circulation, the usual physical signs of impoverished circulation persisting. 
Careful treatment instituted at the very inception of the thrombotic attack, 
may ward off threatening gangrene. 

In short, the prodromal signs of gangrene, namely, symptoms that may 
precede by days, months or years, the development of the mortifying process, 
are in the main: intermittent claudication, paraesthesiae, pallor, cold¬ 
ness, pain, chronic rubor (erythromelia) in the horizontal and dependent 
positions, attacks of thrombosis, blanching in the elevated position of the 
limb or even in the horizontal position, loss of pulsation in the dorsalis pedis 
and posterior tibial, sometimes in the popliteal, more rarely in the femoral 
arteries, and trophic disturbances such as ulcers, fissures, impaired nail 
growth, atrophic skin and edema. 

Amongst the more unusual types of clinical course the following (7 and 8) 
warrant recording. 

7. Cases with Obliteration of All the Pedal Arteries , Popliteals andFemorals. 
After a longer or shorter period of intermittent claudication lasting months, 
sometimes years, severe almost continuous pain may be localized in one or 
both feet, with occasional radiation in the leg or lower thigh. The objective 
manifestations in one case were the following. 


ATHERO- OR ARTERIOSCLEROTIC DISEASE 


387 


The left foot was in a condition of very slight erythromelia, some puffiness of the dorsum 
of the foot and the toes. The leg was markedly atrophic, particularly the muscles of the 
calf, the skin being fairly well preserved. The whole foot seemed to be tender to the touch. 
There was no marked coldness of the foot, except the big toe, the temperature of which was 
manifestly reduced. 

In the dependent position there was fairly marked rubor of the left foot, none of the 
right, although pulsations were absent on the right as well as on the left. On elevation 
there was distinct ischemia of both feet to a slight degree. 

The striking features of this condition are the inability to walk, continuous 
pain in the foot, with atrophy of the corresponding calf, and the absence, of 
all the pulsations in the lower extremities. The difference in the subjective 



Fig. 127.—Arteriosclerotic gangrene. 


and objective manifestations in the two legs of the above case can only be 
accounted for by differences in the development of the collateral paths. 

8 . Chronic Gangrene with Atrophy .—Extensive obliteration of the arteries 
of the lower extremities may lead to a picture of chronic atrophy associated 
with slow development of gangrene that may persist for months or years with¬ 
out infection and without complicating moist gangrene. It is interesting to 
contrast the persistence of large gangrenous areas in these cases, with no 
tendency to inflammatory process in the neighborhood, with the rapid develop- 


388 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


ment of fulminating putrid gangrene in many of the embolic and thrombotic 
cases following infectious diseases and pneumonia. In the latter, possibly 
by virtue of the liberation of ferment, be it through the presence of bacteria 
or their toxins, secondary bland thrombosis develops rapidly in the deep 
veins. In the cases under consideration, however, such venous occlusion is 
absent, and a withered condition without infection ensues. 



Fig. 128.—Arteriosclerotic gangrene. 


It is noteworthy that a senile condition is not necessarily present, and 
the atrophic state may appear in patients in their early fifties or even in the 
late forties. 

An exquisite example of such a process was the following: 

L* S., 54 years of age, does not remember having had any trouble with his limbs until 
the right leg was injured by a fall from a horse (chronic arterial disease, doubtless with 


ATHERO- OR ARTERIOSCLEROTIC DISEASE 


389 


obliteration without symptoms). A wound over the right shin resulted, which necessitated 
a small operation, the nature of which he does not remember. Since then the wound has 
not healed. He has not been able to use the right leg, has been bedridden, and the con¬ 
dition of which he now complains has developed. 

The area operated upon showed no tendency to heal, and a slow gangrenous process 
developed that spread over the greater part of the shin bone, the latter protruding through 
the skin. Until recently almost two-thirds of the length of the bone could be seen through 
the self-enlarging wound. For several months he has also had trouble with the left leg, a 
change in the appearance of the toes having been noted, and the foot being cold. 

Physical Examination, March i, 1921.—Both feet and legs are markedly atrophic 
(Figs. 127 and 128). The anterior aspect of the right leg over the middle two-thirds shows 
extensive dry gangrene of the skin, the antero-lateral and antero-internal surfaces of the 
tibia presenting through a large aperture or defect, being dry, gangrenous, like dry bone 
outside of the body cavity. All the toe nails show hyperkeratosis, discoloration, and there 
is marked atrophy of the skin. At the knee there is an area over the outer condyle of the 
femur, over which the skin has become mummified (dissecting room type). There is 
cyanotic and reddish discoloration of the left foot, and the skin of the whole leg is so 
withered that there seems to be little or no circulation in it, but gangrene is threatening. 

March 14, 1921, amputation of the right leg through the upper third of the right thigh. 
This was followed by sloughing of the flaps. 

During his stay at the hospital the left foot became spontaneously gangrenous, mummi¬ 
fication ensuing. 

April 11, 1921, the patient left the hospital against advice. 

Special Symptoms. Erythromelia of Upper Extremities in Arteriosclero¬ 
sis. —Just as intermittent claudication may involve the upper extremi¬ 
ties (dysbasia angiosclerotica) so also is a condition of rubor occasionally 
observed. Of the author’s atherosclerotic cases with marked rubor of the 
hands or hands and feet, the preponderating number seems to have occurred 
in diabetics. When such erythromelia is a striking phenomenon, then ische¬ 
mia on elevation can also be elicited. As a rule, blanching of the hands is 
relatively more difficult to produce by postural changes than its analogous 
condition in the feet and legs, so that an extensive infringement upon the 
patency of the vascular channels can be prognosticated, whenever rubor and 
pallor are exaggerated in intensity. 

A narration of a typical case may not be amiss here, because of the general 
trend amongst internists to attribute marked rubor of the hands only to ery- 
thromelalgia and other vasomotor neuroses, and because such rubor as an 
expression of compensatory efforts attending organic vascular lesions, is so 
often ignored. 

Atherosclerosis , diabetes , chronic erythromelia of hands and feet. 

Case R. B., Austrian, male, aged 57 years, says he has had diabetes for six years. For 
the last six months the left hand has been swollen. Both hands get red and painful in the 
pendent position. He observed this symptom first in the feet. Six months ago he had 
redness of the tips and borders of the hands; three weeks ago the redness passed above the 
wrist. Warmth seems to increase the pain whilst cold air makes the hands feel better 
There have been no ulcers of the fingers. Eight days ago he had a mild apoplectiform attack 
during which he could not speak for one-quarter of an hour. 

He complains of sticking pains in the borders of the hands and in the fingers with 
neuralgic pains radiating upward. On some days the hands look almost normal and then 
there is no pain. There are exacerbations which last days. 

Physical Examination: Hands. —Both become pale when elevated to 135 0 , and become 
markedly scarlet when hanging down. The redness extends up three inches above the 
wrist on being pendent for a few minutes. There is slight cyanotic discoloration. The 
inner borders are most intensely red. The hands look swollen and puffy, especially over 
the palmar aspect of the left. Both hands feel fairly warm. There are areas of cyanosis 
over the palm, especially over the tips of the fingers. Squeezing the fingers hurts more than 
normally. His hands do not feel better when raised, the pulsations being about the same 
as when in the horizontal or pendent position. Both radial pulsations are absent. 

The brachials and axillaries: Right feels calcareous and pulsation is only felt in the upper 
third. Left also calcareous and pulsation felt in the upper two-thirds. 


390 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Lower extremities : Have the typical appearance of the atrophic condition usual with 
atherosclerotic vessels. Slight erythromelia of the feet in the pendent position; no trophic 
disturbances. 

Femorals: Both exhibit fair pulsation but are very hard. 

Popliteals: Right faint; left absent. 

Posterior tibial and dorsalis pulses not palpable on both sides. 

In the elevated position, even after ten minutes, there is only very slight ischemia. 
Right leg is slightly paler than left. There is only a very slight induced erythromelia, more 
on the left than on the right. 

Erythromelia of Lower Extremities .—The clinical picture of a red painful leg, 
so characteristic of long standing impairment of the circulation attending 
marked atherosclerosis with or without diabetes, is worth mentioning and 
illustrating by a clinical case, for differentiation from thrombo-angiitis obli¬ 
terans and erythromelalgia (Weir-Mitchell) will thereby be clarified. 

Usually, the clinical symptom-complex comprises a history of long standing 
intermittent claudication, with or without previous trophic disorders, possi¬ 
bly an attack of arterial thrombosis without gangrene as a sequela, and 
finally a condition of painful red leg , with atrophy. Edema due to renal 
disturbances or cardiac insufficiency may complicate: 

Erythromelia (red leg) in an arteriosclerotic. 

L. S., male, 83 years of age, has had cramps in his left leg for many years, and 1 year 
ago an attack of severe pain in the left foot. He has been troubled for about 6 months with 
a condition which gives him concern both because of the evident discoloration of the leg, 
and because of the attendant frequent pain and discomfort. His wife says that the 
pain, the redness and the coldness of the leg to the touch are the chief noticeable changes. 

Physical Examination. —The whole of the left foot and part of the leg is markedly red, 
both in the horizontal and pendent positions, the region of the fifth toe being tender. 
Elevation of the limb intensifies the pain in the foot. There is slight edema. The popli¬ 
teal, posterior tibial and dorsalis pedis pulses are absent. There is no gangrene. 

Vasomotor Phenomena. —The nervous mechanism with which arteries are 
endowed and which modifies their reactions to blood pressure, is a potent 
influence wherever local circulatory impairment has taken place. We have 
already alluded to the peculiar vasomotor lability and instability attending 
obstructive arterial lesions. Allbutt 1 is not in accord with the oft repeated 
impression that the superficial vessels in arteriosclerotic cases are even more 
liable to spasm than the healthy. According to this author, plethysmo- 
graphic experiments upon the arm in arteriosclerosis, and observations 
carried out by more than one skilful investigator, 2 - 3 indicate that the response 
of the vasomotor mechanism to stimulation is not enhanced but diminished. 

Whatever the value of artificial methods for gauging the vasomotor 
excitability, the author is convinced from clinical experience that an increased 
susceptibility or tendency to vasomotor phenomena on the part of the small¬ 
est arteries is often present in the cases in which obstructive arteriosclerotic 
disease of the extremities is present. He is in accord with the view that the 
larger arteries do not participate appreciably in effecting the manifestations, 
agreeing, therefore, with Albutt in this regard. But in the more peripheral 
arteriole and capillary territory, a distinct accentuation of vasomotor 
fluctuation occurs that suffices to give noticeable symptoms. 

Trophic Disturbances and Gangrene— It is important to distinguish 
between the two large groups of tissue disintegration, which result from 
imperfect and arrested circulation, first trophic disturbances , and second, 
gangrene. 

[I 1 Allbutt, Diseases of the Arteries (Macmillan, 1915). 

2 von Romberg, Deutsch. med. Wchnschr., Oct. 28, 1909. 

3 Muller, O., Deutsch. med. Wchnschr., 1906, 38-39. 


AT HERO- OR ARTERIOSCLEROTIC DISEASE 


391 


1. Trophic Disturbances. —Trophic disturbances include all manifesta¬ 
tions of impaired nutrition of the skin and its adnexa, and may develop 
months or years before gangrene is established. They occur much less 
frequently in arteriosclerosis than in thrombo-angiitis obliterans. 

The skin may be atrophic or withered, and the nails may show evidence of 
impaired growth. Ulcers at the tips of, or between the toes, the sequelae 
of abrasions or small wounds, are occasionally found. More rarely, punched 
out indolent ulcers over the dorsum of the foot, or over the lower half of the 
leg, may be complications of attacks of extensive thrombosis. 

Small bullae, the precursors or prodromal signs of small patches of 
gangrene, may lead to ulcers or to the separation of a nail. They may heal, 
or may lead to extensive gangrene. Perforating ulcers more often attend the 
diabetic cases of arteriosclerosis, and are to be found most frequently over 
the plantar aspect of the foot. They are chronic in their course, and often 
associated with deep necrosis and suppuration. When they involve the 
toes, they lead to necrosis of bone. The toe may become enormously 
enlarged. A granulating strawberry-like wound may be formed, which lies 
at the orifice of a tract leading down to dead bone. 

A bunion at the metatarsophalangeal joint of the great and fifth toes, 
not infrequently affords a good nidus for an ulcer which almost always leads 
to necrosis of the underlying bones. 

Small ulcers, of the perforating variety, near the base of a toe, often 
represent the orifice of penetrating abscesses, the necrotic and suppurative 
process extending along the tendons and bone, and causing necrosis of bone 
for a considerable distance beyond the site of the wound. 

In the case of the upper extremities, trophic disorders associated with 
arteriosclerosis are very rare, and their presence should, therefore, suggest 
either the existence of thrombo-angiitis obliterans, vasomotor disease, or 
other neuropathic cause. Gangrene, too, of the upper extremities is exceed¬ 
ingly rare, though a symptom-complex comparable to intermittent claudica¬ 
tion in the lower extremities is occasionally encountered. In rare cases 
there may be intense rubor of the hand. The radial artery may fail to 
pulsate and can be palpated as a rigid cord. X-ray examination will reveal 
intensely calcified arteries, or at least calcareous deposits along the course 
of the larger vessels. 

2. Gangrene. —Although it is most commonly seen in the aged and, 
therefore, has been termed senile gangrene (chronic or Pott’s gangrene), it 
may also afflict younger individuals between the ages of 40 or 50, when the 
atherosclerosis is precocious in development, or when a secondary thrombosis 
occurs early in the disease. In most instances dry gangrene develops. In 
some, however, we may see the moist type or combinations of the two. 

Dry gangrene usually involves the toes, the big toe being the site of pre¬ 
dilection. Or, there may be multiple areas of gangrene involving the 
peripheral parts, and in the more severe cases, extensive dry gangrene of the 
greater portion of the foot may be expected. The process may be a slow one, 
the toes being spontaneously amputated or removed by operation. The 
extent of the gangrene cannot be exactly estimated in the atherosclerotic 
and diabetic cases, from the external appearances, nor from the line of demar¬ 
cation when it is present. For, if such an amputated limb be dissected, 
extensive, widespread sloughing of the deeper tissues with necrosis of bone 
extending for a considerable distance beyond or above the apparent line of 
limitation, will often be revealed. It is incumbent upon us, therefore, in 
every case to make an X-rav examination of the foot, as this may demon- 


392 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


strate that the destruction has implicated tissues beyond the zone of skin 
involvement. 

Where infection is superadded, the usual signs of phlegmon formation 
or lymphangitis will be in evidence. The suppurative inflammation will 
spread into the healthy tissues from the site of the gangrene, either in acute 
fashion, or subacutely without causing any considerable rise of temperature, 
but evoking intense pain. 

Moist Gangrene .—Early evidences of threatening gangrene will be intense 
cyanosis, coldness of the affected part, usually the toe, and the appearance 
of a hemorrhagic bleb or a number of blebs filled with pinkish serum. The 
part will have a dark bluish or purplish appearance, or even angry red where 
the epidermis becomes lifted off. In the immediate neighborhood, there 
will be ecchymoses over smaller or larger areas, and edema with exquisite 
tenderness just above the mortifying tissues. Where there is infection, the 
typical signs of lymphangitis usually following the course of the internal 
saphenous veins will be encountered. In later stages the epidermis becomes 
detached, is folded, and hangs loosely in places. 

In some cases there will develop spontaneously a number of large bullae 
over the toes or dorsum of the foot, and, in these, clear or bloody serum alone 
will collect. This is the early stage of moist gangrene. As the gangrenous 
process extends, all those changes that have been previously cited and de¬ 
scribed under moist gangrene will make their appearance. If infection occurs, 
the phlegmonous process is more rapid and intense than in the case of dry 
gangrene, and particularly in diabetic cases will the resistance on the part 
of the body be inadequate, and the inflammatory process difficult to check. 

Clinical Course in Athero- or Arteriosclerotic Disease. —Although the 
variations from the given types are manifold, and it is, therefore, impossible 
to recount all the various types of clinical course, the following summaries 
include the most common. Many patients have intermittent claudication 
and pain on walking for a long time, then develop coldness of the toes or of the 
whole foot, paresthesiae, but rather rarely are afflicted with ulcers or other 
signs of trophic disturbance so characteristic for the disease, thrombo-angiitis 
obliterans. They may have attacks of thrombosis, complicated with ulcers or 
patches of gangrene, or such attacks may be followed by healing and a state 
of chronic erythromelia with discomfort and some disability in the affected 
leg; or, practically all symptoms may be absent until after some insult, 
traumatism or cold, or without cause a patch of dry or moist gangrene 
develops. In a number of cases, particularly in the diabetic, a perforating 
ulcer brings the patient to our notice, and this is complicated by necrosis of 
bone and the usual signs of deep infection. Many patients complain only of 
disability, particularly diffculty in walking. Some develop an, ulcer of the 
nail-bed with a patch of dry gangrene that heals. 

Others never develop gangrene, but the signs of insufficiency of circulation 
are manifest if the limbs be examined as, blanching on elevation, slight 
erythromelia, and absence of pulsation are regularly present. 

The author has made an observation that these latter patients are prone 
to fugitive attacks of erysipeloid infection of the feet and legs, or mild lymph¬ 
angitis with short periods of fever. Perhaps diminished resistance of the 
inadequately nourished territories predisposes to such complications. 

When gangrene develops—usually of the dry variety—the onset is often 
ascribed to some previous injury, the paring of a corn, the wearing of too tight 
a shoe, exposure to cold, a bruise or the application of some strong medicament. 
The big toe is usually the first to be involved. Its tip or the whole of it 


ATHERO- OR ARTERIOSCLEROTIC DISEASE 


393 


becomes dusky red or purple, gradually becoming purplish-black. These 
changes in color and evidences of mortification are attended with intense pain 
in the affected region and in the foot. If the gangrene remains dry and no 
infection takes place, mummification ensues, the toe becoming dry and 
shriveled, into a hard black mass This, however, may be associated, as 
referred to above, with necrosis and suppuration in the depth. A line of 
demarcation may form, or gangrene may spread, depending upon the presence 
or absence of infection, the resistance of the tissues, and the condition of the 
arteries. 

Clinical Forms of Trophic Disorders and Gangrene. —So variegated are the 
clinical pictures presented by the various types of nutritive disorders com¬ 
plicating arteriosclerotic closures of the vessels of the extremities with or 
without thrombosis, that but a very few types can be mentioned here. 

The following review will aid the clinical recognition of this condition. 

1. After the removal of a corn by the chiropodist or by the patient himself, 
or after the slightest cutting injury a small focus of pus develops, the toe 
becomes red and cyanotic either through inflammation or stasis, and gangrene 
of this part soon ensues. 

2. A blister or larger bulla that is more than usually painful develops over 
a t:>e, or on the dorsum of the foot, the epidermis is cast off leaving a discolored 
derma which becomes bluish black, and then gangrenous. 

3. Or, the bed of the nail begins to bleed, possibly attended with the 
formation or a blister or bleb at the distal margin of the nail, or with more or 
less chronic suppuration. And finally, when the nail becomes completely 
separated, the gangrenous area or extensive slough is seen to lead down to 
bone. 

4. After a longer or shorter period of prodromal symptoms, particularly 
intermittent claudication, chronic blueness or cyanosis affects some of the 
parts, particularly the big toe. Days or weeks pass, then ulceration and 
gangrene terminate the picture. 

5. Although the big toe seems to be the site of predilection in arterio¬ 
sclerotic cases, gangrenous patches may develop anywhere: over the dorsum 
of the foot, over the heel, often in the neighborhood of calluses or fissures. 
When these become infected, attacks of lymphangitis or deeper infections are 
not infrequent complications. 

6. Atypical forms of ulceration of the indolent type are not uncommon. 
Multiple ulcers were observed in a case that gave a typical history of inter¬ 
mittent claudication and pain in the feet, there being marked ischemia and 
intense erythromelia. There were shallow, punched out, indolent ulcers over 
the dorsum of the foot, most of them no larger in diameter than a quarter of an 
inch, the result of the separation of the gangrenous patches of skin, their margins 
showing no tendency to heal, and no reactive hyperemia. Such ulcers may 
persist for a long time until finally, by reason of a fresh accession of thrombo¬ 
sis in the deep vessels, or some mechanical or thermal cause, extensive gangrene 
of the foot occurs necessitating amputation. 

7. Occasionally there is a history of the existence of previous ulcers that 
have healed, with a complete repetition of the clinical course. 

8. The big toe may be found in a condition of chronic granulation and 
ulceration, being enormously enlarged, almost twice the size of normal, 
presenting a large granulating strawberry-like surface at the center of which 
a sinus may lead to dead bone. 

9. A type is also encountered in which trophic disorders in the form of 
ulcers are present, is followed later by dry gangrene involving all the toes. 


394 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Hemorrhagic or purple spots appear, are painful, and then may become the 
seat of gangrene. 

10. The whole foot may be in the state of very intense erythromelia, it 
being almost a vermilion red, except over the area of trophic disturbances or 
gangrene when such are present. Many of the various forms of trophic dis¬ 
orders maybe associated with this intense rubor. 

11. Cases with patches of dry gangrene give a history of discoloration and 
pain over periods of weeks or more. A small purplish or cyanotic spot 
develops, particularly over a toe, and then this process after the elapse of 
many days, may extend rapidly over to the rest of the toes and foot and 
eventuate in a condition of dry gangrene. 

12. A type with extensive dry gangrene, shows mummification of all of the 
toes, and portion of the dorsum, as well as the sole of the foot. The rest of the 
foot, when not involved, is very cold, presenting a cyanotic and hemorrhagic 
discoloration. In other cases where the line of demarcation is distinct, there 
is no evidences of progressive gangrene above the line. In addition to the 
large area of gangrene, corresponding areas of poor circulation are found. In 
other cases there is complete ischemia for a distance above the demarcation, 
or hyperemia depending upon the condition of the circulation. 

13. Cases with the development of moist gangrene usually develop large 
blebs over the dorsum of the foot and toes, the various toes showing different 
types of lesions. There may be extensive cyanosis of the toes, coldness, with 
blackish discoloration. The epidermis becomes lifted off by a collection of 
serum and blood, and certain toes show only cyanosis or black blebs, all of these 
being in various stages of the gangrenous process. If inflammation is present, 
intense hyperemia of the dorsum must be distinguished from the erythro¬ 
melia. The dorsum of the foot also may show discrete patches of gangrene, 
cyanosis and hemorrhagic blebs. Phlebitis and lymphangitis may accompany 
this picture, so that when a cross section is made along the course of the in¬ 
ternal saphenous vein after amputation, pus can be expressed out of the 
lymphatics. 

14. Cases with chronic gangrene and atrophy. Where the limb or limbs 
become wasted and almost shrivelled up, a chronic form of gangrene lasting 
for a year or more may give a remarkable picture. In such cases the greater 
part of the tibia may present in dried form through a large wound that is the 
result partly of trauma or the result of whatever cause. The foot or feet 
may be almost intact, with, or without gangrene of the toes, but atrophic, cyan¬ 
otic or red, with the patient bedridden for months and years. 


CHAPTER LXVII 

ARTERIOSCLEROSIS—PATHOLOGY 

Pathogenesis.—Arteriosclerosis according to Marchand 1 is a deteriorative 
disease of the vessels. Because of the exquisite fatty changes that occur 
in the vascular walls, the affection was termed “atherosclerosis” in contra¬ 
distinction to the old name “arteriosclerosis.” The latter term was first 
employed by Lobstein in view of the hardening of the] vessel wall. The 

1 Marchand, Verhandl. d. 21 Kong. f. inn. Med. 



A R TERIOSCLEROSIS—PA THOLOG Y 


395 


appellation “endarteritis” was coined by Virchow as descriptive of a reactive 
hyperplastic lesion of the intima. 

The more recent observations of several authors (Jores, Marchand and 
others) interpret arteriosclerosis or atherosclerosis in the light of effects of 
deterioration resulting from stresses and wear. Marchand views athero¬ 
sclerosis as a progressive nutritional disturbance of the vessel wall, accom¬ 
panied by thickening and sclerosis of the intima, multiplication and 
degeneration of the cellular elements, partial necrosis, and finally disintegration 
and calcareous degeneration. In the arteries of the extremities the media is 
particularly implicated in the degenerative process. 

Recent authorities lean to the view that the peculiar alterations are the 
results of nutritive derangement, that is evoked by the excessive functional 
stresses. In this sense one would interpret atherosclerosis rather as a 
deteriorative disease due to wear and excessive use, rather than as purely a 
senile change. The deleterious factors (mechanical factors) do not usually 
attain sufficient intensity until a certain age is reached; for, cumulative 
action through many years is required to bring about the necessary arterial 
responses. From the varied distribution of the process in the vascular 
system, it would appear that the individual suffers in those vascular territories 
which are most subject to strain in the respective case. 

In the light of most recent investigations, the proliferative and degenera¬ 
tive processes in the intima and media are expressions of the same disease, and 
the very histologic forms depend upon the particular structure and function 
of the vessels involved. 

In the evaluation of such a deteriorative disease, we must not forget that 
the end products, we are wont to see, are elaborated over many years. To 
investigators, such as Aschoff, 1 must be given considerable credit, for their 
demonstration of the manner in which the characteristic changes are produced 
from the normal embryonal arterial types up to the markedly degenerative 
senile products. The arteries are in no essential sense different from other 
organs in which the process of building up attains a certain climax, and in 
which the process becomes stationary for a certain period, only to undergo 
regressive subsequent deterioration. Furthermore, it is known that the 
structural development of the various organs attains its height at varying 
periods and this seems to be true also in the arterial system. Aschoff 
through his embryological studies demonstrated clearly that a comparison 
of the embryonal arteries with the pictures they offer during early infancy, 
afford enough similarity to warrant the assumption that the later changes 
are but intensifications of these with secondary regressive degenerative 
lesions. 

It would seem well, therefore, for a clear understanding to approach the subject with a 
description of the arteries of the embryo, those of the child, and those of the adult. For this 
the reader is referred to the chapter on Histopathology of Arteriosclerosis. 

We need not discuss here the many theories as to the pathogenesis of 
athero- or arteriosclerosis. Histologic studies have demonstrated that the 
beginnings of arteriosclerosis are recognizable even during youth. These, 
however, do not necessarily develop into a diseased process. The alterations 
that correspond to the aging process do not constitute a disease per se, but 
a manifestation of deterioration. Although all individuals show the well 
known evidences of arterial deterioration, only some develop a progressive 

1 Aschoff, Ueber Entwick. Wachs. u. Alt. Vogange a. d. Gefassen, (Fischer—Jena, 1909). 


396 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


process of sufficient intensity to be regarded as true arteriosclerotic or athero¬ 
sclerotic disease. 

Potent as the mechanical stresses may be in the production of the degen¬ 
erative and hyperplastic changes in the arteries, these moments, as well as 
those of deterioration, cannot altogether explain all of the histologic changes 
observed. If we extend the term deterioration to include all of the influences 
that arteries are exposed to during life, we have a term so comprehensive that 
it would naturally include forces of diverse variety. As such, deterioration 
would include a complex of influences, in which not only physical, but also 
chemical factors, would be engaged. In addition to the generalized wear 
and tear that all tissues undergo, the arteries must be affected (Hueck) by 
additional factors in order that the lesions known as athero- and arterio¬ 
sclerosis be elaborated. Nor can we accept the view that the causal moments 
must necessarily be uniform in all cases. Perhaps the special changes, such 
as calcification, depend upon additional toxic factors. Therefore, in this 
complicated problem it is impossible to estimate to what extent each of the 
many causal moments participates in the production of the end result. 

The researches of Jores 1 because so important, deserve more than mere 
passing mention. According to this author, the changes in the intima 
although not the only lesions of arteriosclerosis, are the essential alterations; 
and an explanation of the intimal thickening will also throw light on the 
pathogenesis of the whole process. 

Heubner from a comparative study of syphilitic endarteritis of the brain arteries and 
arteriosclerotic vessels, had concluded that the latter process suggests true hypertrophy 
of the intima with proliferation of existing elements, especially the elastic lamella, so that 
the architecture of the intima of small arteries approaches that of the normal larger ones. 
All the secondary processes, such as fatty degeneration, calcification, are to be considered 
essentially regressive in character, and as unimportant in so far as pathogenesis is concerned. 

Jores has laid special emphasis on two types of elastic lamellae in the 
intima. The first variety shows reduplication of elastic fibers in a manner 
that suggests a cleavage of the membrana interna elastica, with splitting 
off of fibers, and is characteristic of the arteriosclerotic process. In the 
second type, new formed fibers of more delicate composition appear. 

The author in his first publications on the histopathology of thrombo¬ 
angiitis obliterans 2 had noted and emphasized the difference between the 
new formed elastic fibers in the obliterating tissue of thrombo angiitis obliter¬ 
ans, and those so peculiar to the hyperplastic lesion of arteriosclerosis. So 
also, Jores had observed a similar discrepancy in the thrombosed arteria 
fossae Sylvii of a case, and in the experimentally produced endarterial 
lesion following ligation. The aforementioned peculiarities are specific in 
his opinion. The hyperplastic intima associated with certain thromboses 
and ligation, shows also a multiplication of elastic elements. But this corre¬ 
sponds to the proliferation seen under other circumstances and in other 
tissues. The process characteristic of arteriosclerosis is initiated by thicken¬ 
ing of the internal elastic lamina and consequent cleavage, a lesion that has 
no analogy elsewhere in the body. 

Elastic Fibers in the Normal Arteries .—For a correct comprehension of 
the pathology of elastic fibers of the arterial intima, a knowledge of the 
normal is a sine qua non, especially since variations in the thickness of this 

1 Jores, L., Wesen u. Entwickelung d. Arteriosklerose, Wiesbaden (J. F. Bergmann), 
1903. 

2 Buerger, Pro. N. Y. Path. Soc., Feb. & Mar., 1908. 


ARTERIOSCLEROSIS—PA THOLOGY 


397 


coat, its elastic fiber content and even reduplication of these lamellae may 

occur. ... , n r 

In the newborn and in young infants, the intima is made up merely ot 
the internal elastic membrane, and the endothelium. A musculo-elastic 
layer is only found at the bifurcations of the small arteries. Where vessels 
are given off, small protuberances made up of such tissue project into the 
vessel lumen. A longitudinally disposed muscle layer is inserted, as it 
were, at certain places between two laminae of the internal elastic mem¬ 
brane. Of the two elastic layers, the inner is more prominent than the 
outer, and conserves the general course of the vascular fibers. Within 
these elastic lamellae are enclosed not only the longitudinal muscle bundles 
above noted, but also finer elastic fibers. This complex structure in its 
entirety simulates, as can be readily seen, the lesion of intimal thickening 
characteristic of the arteriosclerotic process. 

Although first limited to the wall near the angles of vascular offshoots, 
the duplication of elastic fibers soon extends longitudinally, so that cross 
sections will find it at situations independent and far removed from points of 
bifurcation. Spreading even in a circular direction, pictures are produced 
in which a greater part of the circumference of the vessel wall is occupied by 

this process. . _ , 

Such normal variations of the internal elastic membrane do not appear 

to vary in intensity according to age. . , ,, p ^ 

In short, a thickening of the intima indistinguishable from that occurring 
under certain pathological conditions, is elaborated in the normal, probably 
as a reactive response to functional demands. . . , 

Both in physiological and pathological hypertrophy of the mtima, there 
is a concomitant appearance of nuclei between the layers undergoing cleav¬ 
age. It is a mooted question as to whether the longitudinally disposed cells 
lving between the elastic lamellae are muscle cells or not. In fact, m longi¬ 
tudinal sections, an intima of considerable thickness is sometimes suggestive 

of a muscular media. . . , . , _ 

We have learned to recognize therefore, two criteria of the normal pro¬ 
ductive variations in the intima, first the elastic tissue alterations and 
secondly the muscular inclusion which manifests a characteristic homo¬ 
geneity. If we contrast here the composition of the intima accompanying 
thrombotic processes, we will note the absence of muscular elements. 

A third distinctive differential point between the pathological and the 
normal is the occurrence of alterations in the media which attend not only 
arteriosclerotic processes with thrombosis or calcification, but also are 
found in thrombo-angiitis obliterans and arteries after ligation, or the seat 
of embolism. These are the infiltration of the media with connective tissue, 
and a striking vascularization or invasion with new formed vessels, and are 
evidences of the participation of the vessel wall in the reactive processes 
incident to morbid changes affecting the intima and artenal patency. 

The author 1 too, has described such morphological alterations in the 
media of the arteries in thrombo-angiitis obliterans, calling attention to the 
teleological penetration of vessels into and through the muscular co 
through which they can enter or send sprouts into an occluding clot, and 
partake in its canalization and connective tissue transformation. 

Much discussion has arisen and contentious explanations are many on 
the relative roles of the media and intima in the incitement as well as actual 

i Buerger, Proc. N. Y. Path. Soc., Feb. & March, 1908. 


398 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


participation of intimal hypertrophy. The weight of evidence, as also 
observations of the author, strongly attest to and confirm the importance 
of the media and adventitia in the thickening of the intima as well as in 
the metamorphosis of occlusive parietal thrombi. 

Jores 1 recognizes firstly an intimal enlargement in which the reduplication of elastic 
fibers has its origin in the existing lameliae, and secondly, a form in which proliferation by 
virtue of agencies acting from without (media and adventitia) inward are potent. Views 
are divergent as to whether the activating factor in the latter is of inflammatory nature or 

not. c . . 

As for the source of the new formed elastic fibers, contradictory expressions ot opinion 
are found amongst pathologists. Whilst Jores assumes that new formed elastic fibers 
must emanate in the first type (which he calls hyperplastic thickening of the intima) from 
the internal elastica, and in the second form (to which he applies the term “regenerative 
proliferation”) from prolongation and hyperplasia of existing elastic fibers of the media, 
and, whilst he desires to controvert the theory of metaplasia from connective tissue as a 
mode of production of such tissue, the author has shown that so restricted a view is un¬ 
tenable. For, newly formed elastic fibers appear around and encircle the new vessels in 
the center of the organized occlusive thrombus, at situations widely removed, and in no sense 
continuous with similar fibers of the media or intima. Such neoplastic vessels, it is true, 
arise from new formed capillaries that may represent prolongations from similar structures 
in the media, but the elastic fibers about them could not [have been carried in by the 
angioblasts from which the older vessels were born and had matured. This special 
perivascular distribution in the author’s opinion, speaks in favor of the following view: 
That elastic tissue fibrils are made out of the collagenous connective tissue elements 
(metaplasia?) by a stimulus derived from the endothelial cells; and that that impulse bears 
a direct relation in intensity, to the intravascular carrying power of the vessel enclosed by 
the new formed lamellae; that the endothelial cells themselves do not produce elastic tissue 
is fairly certain, but that they predetermine the elaboration and distribution of such tissue 
is more than likely. The older and larger the new vessels in the thrombus of thrombo¬ 
angiitis obliterans, the more elastic elements are formed. 

Although this view is not in accord with that of Jores, it finds adequate support in the 
abundant material elsewhere described (Chaps. LXI and LXII). That this author’s 
concept of the varied arterial lesions is limited by lack of experience with that most instruc¬ 
tive form, thrombo-angiitis obliterans, is confirmed by his own words. In the passages on 
arterial lesions of “spontaneous gangrene,” he says: “Ueber diese Erkrankung stehen 
mir eigene Beobachtungen nicht zur Verfiigung” (“I have made no personal observations 
on this disease”). From his perusal of the literature, which we have elsewhere demon¬ 
strated tol contain fallacious and misleading interpretations, Jores concludes that the 
lesions are’to be grouped under his form of “regenerative hyperplasia.” 

In arteriosclerotic vessels, Jores recognized both varieties of intimal change, the purely 
hyperplastic with not only reduplication by cleavage, but also by true proliferation; and 
the second type of regenerative connective tissue growth in the intima, or combina¬ 
tions of the two. Often the separated elastic lamellae enclose new formed connective 
tissue which may include foci of degeneration. 2 

Jores emphasizes the importance of the finding of two histologically separable and 
diverse types of intimal change, postulating for these different causal agencies. Such a view 
he holds to be contradictory to the accepted 3 uniformity of explanation for the vascular 
lesions in this disease. . 

The theory that inflammation is responsible he considers untenable, since the typical 
hyperplastic manifestations occur in normal arteries, are seen in children and are unaccom¬ 
panied by any of the usual histological structural elements of inflammatory processes. 
Since this type of intimal thickening is the predominant one in arteriosclerosis, the inflam¬ 
matory theory is incompatible with the appearances described by the afore-mentioned. 

The Hyperplastic Intima .—As for origin of the type with cleavage of 
elastic lamellae, two hypotheses may be entertained. Firstly, we may regard 
the overgrowth of the intima as a physiological response, and that this proc- 

1 Jores, Loc. cit. 

2 That this view is incorrect, the author’s researches on thrombo-angiitis obliterans have 
conclusively demonstrated. 

3 That is, up to the year 1903 when the monograph of Jores appeared. 


A R TERIOSCLEROSIS—PA THOLOG Y 


399 


ess extends itself in arteriosclerosis, becomes more intense, suffers attendant 
fatty degeneration and connective tissue infiltration. 

Secondly, a non-physiological basis may be considered. One may 
suppose that there are noxious influences that are present to a greater or 
less degree in all persons, causing intravascular lesions in certain of them 
with the aid of other predisposing factors. The irregularity of the dis¬ 
tribution of the foci of intimal hyperplasia in the very young and the absence 
of such a change in the embryo would speak in favor of such a view. Then, 
too, the gradual transition into the degree considered pathological is of 
moment. 

Such an injurious element leading to hypertrophy of the intima is in all 
probability an increased functional burden or augmentation of the normal 
intravascular pressure. If we consider that there is often a distinct quanti¬ 
tative relationship between the hypertrophy of the longitudinal muscular 
fibers and the thickening of the intima, this theory obtains additional 
support. 

According to Fuchs, 1 amongst the developmental irritants for the vascular wall, that 
is, of the factors influencing growth, a periodic, physiologic, rhythmic impulse is important. 
An increase in pulse tension is to be regarded as such. If we transfer this hypothesis to 
the conditions in which the physiological passes over into the pathological, we can assume 
that both hyperplasia of the intima, as well as the longitudinal musculature can follow 
in proportion to the degree of abnormal physiological irritants. 

Genesis of the Regenerative Connective Tissue Proliferation of the Intima. —There is no 
doubt but that connective tissue growth in the intima may be associated with or without 
inflammatory processes. In arteriosclerosis both lesions of intima and media with their 
concomitant fibroses would seem to owe their existence to some other than an inflammatory 
motivating agent. 

The researches led Jores to conclude that hypertrophy of the intima pre¬ 
cedes the arteriosclerotic process, which in the aorta is comparable to the 
hyperplasia of the first years of extrauterine life and is attended with hyper¬ 
trophy of the musclo-elastic longitudinal layers. 

The hypertrophic intima with the musculo-elastic longitudinal layers, 
tends to undergo fatty degeneration. As a result there follows a proliferation 
of connective tissue which may be diffuse or circumscribed depending on the 
extent of the degenerative foci. Since all diffuse fibroses of the intima are 
not of arteriosclerotic nature, and since a diffuse endarteritis fibrosa whose 
causation and significance are still unknown, can occur, other characteristics 
must be sought to differentiate and stigmatize the arteriosclerotic lesion. 
Such are the participation of a hyperplastic intimal layer with fatty metamor¬ 
phosis of the latter, and the development of a connective tissue ground sub¬ 
stance between the elastic lamellae. 

An increased functional demand on the arterial wall seems to be the 
sine qua non for the origin of the arteriosclerotic process. In respect to the 
nature of this change from the normal physiological, intravascular, mechani¬ 
cal and hydrostatic conditions, heightened blood pressure with its concomi¬ 
tant increased tension of the vessel wall would seem to offer the most 
satisfactory explanation. Whatever impresses itself upon and especially 
influences longitudinal musculo-elastic layers of the vessel wall to an excessive 
degree, would be the most probable motivating agent in the calling forth 
of structural responses, manifested as 11 arteriosclerotic .’ 1 

Experiments in which the intracanalicular pressure in rubber tubing or 
a hose is altered, give valuable information for deduction. Let us inject or 

1 Fuchs, R. F., Zur Physiologie u. Wachsturms Mechanik des Blutgefass-systems. 
Habilitationschrift, Jena, 1902. 


400 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


force into an elastic tube an increased amount of fluid. We will find that not 
only will the tension increase, but a lengthening will take place, showing itself 
in a motion of the whole tube. In the arteries the circular muscular coat 
whilst in a state of tonicity or contraction, easily limits the expansile increase 
of pressure (felt as pulse), whilst the mechanically more restricted action of 
the longitudinal fibers permits of considerable elongation of any given 
arterial length. This manifestation is clinically observable in the tortuous 
temporal arteries. In these an elongation with increasing age and a ser¬ 
pentine motion transmitted by each heart beat are well known phenomena. 

Excessive pressure then would seem to make even greater demands in 
the longitudinal elements than on the relatively stronger circular ones; and 
consequent reactive hypertrophic changes characterized as arteriosclerotic 
would be the vascular response. 

Experimental Arteriosclerosis.—Because the arteries are under the 
influence of so many varied factors, partly hydrostatic, partly pulsatile 
forces and constantly changing intravascular stresses, and since they are 
subject to the chemical influences of the blood (toxic and bacterial) the 
possible components making for pathologic alterations are indeed many. 
Considerable experimental work has been done in animals with a view to 
reproducing some of the pathologic alterations seen in the human, particu¬ 
larly the athero- and arteriosclerotic. It may suffice here to recount in 
brief some of this work, in order to point out the manner in which possible 
etiologic factors should be interpreted. 

In the attempt to produce arteriosclerotic changes most experimental 
work has failed, in that an exact reproduction of the typical alteration has 
not been possible. However, interesting results followed the administra¬ 
tion of adrenalin products in animals. It has been possible to bring about 
distinct changes in the arteries. Most of the authors agree with the find¬ 
ings of Josue. 1 The changes comprise whitish areas and granular changes 
in the intima of the aorta; streaks and larger areas of thickening of the same 
region, with precocious calcification; discrete or confluent lesions, with partial 
umbilication; and aneurysm formation of varying size up to that of a bean. 
The lesions vary in size from microscopic up to plaques about 0.5 cm. in 
diameter. 

Microscopically it was found that a primary change occurred in the media, particularly 
in its central two-thirds. This is said to be typical, extending in plaque-like fashion 
through the muscular coat, and on cross section appearing as small streaks or segments of 
a circle. 

The muscle cells show their degeneration in the loss of tinctorial properties, fragmenta¬ 
tion and loss of their nuclei. Most investigators admit that a necrosis of the muscle cells 
occurs. 

Klotz 2 mentions that fatty degeneration of the muscles is regularly initiated by adrena¬ 
lin injection. According to his view neutral fat is first formed; this is converted into fatty 
acids, and these later produce insoluble soaps with the calcium of the blood and lymph. 

Saltykow 3 on the other hand, regards the fatty conversion to be inconsequential, the 
essential process being the necrosis. 

The elastic elements are said to undergo characteristic changes. The lamellae in the 
neighborhood of the foci lose their undulatory course, approach each other and seem to 
become somewhat agglutinated. Others (Kiilbs 4 ) speak of a separation of the elastic 
fibers. The lamellae show granules, stain poorly, may tear, become fragmented or split. 
Finally they undergo degeneration and may disappear. Klotz refers to such degenera- 


1 Josue, Presse med., 1904, S. 281. 

2 Klotz, Jour. Exper. Med., 1906, 8, p. 322; also p. 504. 

3 Saltykow, Centralbl. f. allg. Path. u. path. Anat., 1908, XIX, p. 321. 

4 Kiilbs, Verhandl. d. XXII deutsch. Kong. f. inn. Med., 1905, p. 246. 


A RTERIOSCLEROSIS—PA THOLOGY 


401 


tion. Calcification is an early process; sometimes the specific foci are visible only 
microscopically. 

The Intima .—Proliferation of the endothelium is mentioned by Kiilbs and Saltykow; 
others speak of degeneration of the endothelium; and still others regard the intima as 
thickened with normal endothelial cells covering it (Scheidemandel). The changes in the 
intima may precede those in the media (Papadea 1 ). Ziegler interprets the irregularities of 
the inner surface of the arteries as due to hypertrophy of the intima. 

The Adventitia and Vasa Vasorum .—Changes in the adventitia are either absent or may 
be of a reactive nature, with perivascular infiltration. According to Orlowsky 2 the chief 
changes in the arteries are due to an obliterating endarteritis of the vasa vasorum; and 
others recognize a similar process with complicating hyalin thrombosis (Trachtenberg 3 * ). 

Summary .—The essential changes in adrenalin atherosclerosis seem to 
be in the media, and the thickening of the intima is secondary. Perhaps 
the latter is a compensatory or reparatory process due to the weakness 
of the media. Opinions differ as to whether the primary changes occur in 
the muscle cells or in the elastic element. The weight of evidence leans 
towards the view that the muscle cells are first implicated, although a number 
of authors lean to the other contention that the elastic elements are first 
damaged. 

As cause of the arterial changes a number of different explanations are 
given comprising the following: Increased blood pressure due to the action 
of the adrenalin extract; a direct elective toxic action upon the muscle 
elements of the media and closure of the vasa vasorum, with secondary 
trophic derangements of the media; or a combination of both causes. 

The Relation of Human and Experimental Atherosclerosis.—Critical and comparative 
investigations by a number of authors have led to the conclusion that changes in the arteries 
of the rabbit due to adrenalin experiments, show characteristic differences from those lesions 
of human atherosclerosis. Distinctive features in the human are the essential localization 
in the intima, the degree of fatty degeneration and the subsequent calcification, as the final 
stage of the regressive process. In the experimental rabbit, on the other hand, there has 
been noted the special localization in the media, a relatively small degree or absent fatty 
degeneration, and calcification at the very inception of the disease. 

It is still a mooted question as to whether the alterations following adrenalin injection 
are attributable to a specific toxic action, or indirectly through the increased pressure 
occasioned. That a direct action may play a role, has not as yet been controverted. 

Experiments with nicotin and tobacco have not been convincing; and, although authors 
report lesions similar to those produced by adrenalin, the resemblances between the artificial 
and the human lesions are not sufficient to permit of positive conclusions. 

Experiments have also been made with various chemical substances and bacteria. 
The injection of the latter has not resulted in the formation of arteriosclerotic changes. 
Saltykow and Klotz, however, report changes not unlike those of human atherosclerosis 
after injection of micro-organisms (staphylococci and streptococci). The lesions were 
found in the aorta and included fatty degeneration, proliferation and degeneration of the 
subendothelial layers. In Saltykow’s rabbits the degenerative changes were so marked that 
he speaks of them as being easily mistaken for the human atherosclerotic processes. 

Localization of Arteriosclerosis.—The localized incidence of arterio¬ 
sclerosis as it invades the arterial tree accounts for the frequent clinical 
confinement of manifestations to the extremities. The factors productive 
of the lesions are variable in that the stresses in the members include a 
number of different concomitant agencies. To what extent each of the 
determinants, such as static influences, motion, locomotion, the special 
affinities of toxins, and others, contribute, cannot be accurately ascertained. 

1 Papadea, Riv. di patol. nerv., 1906, Vol. II, fasc. 5. (cit. by Tarantini in Policlinico, 
1906, Sez. med., Vol. XIII, p. 311). 

2 Orlowsky, Russk. Vrach., 1905, p. 1443; a l so I 9 ° 7 > P- 3 6 4 - 

3 Trachtenberg, Charkower med. Jour., 1907, III p. 468. 

26 


402 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Concerning the sequence and frequency in which this process affects the arteries, there 
seems to be little or no unanimity of opinion. The order given by Albutt based upon 
statistics of Thoma’s material is: ulnar (94 per cent), anterior tibial (93 per cent), sub¬ 
clavian (88 per cent), cerebral (87 per cent), internal carotid (87 per cent), radial (86 per 
cent), splenic (82 per cent), popliteal (79 per cent), axillary (71 per cent), femoral (87 per 
cent), common carotid (68 per cent), ascending aorta (67 per cent), abdominal aorta 
(64 per cent), external iliac (58 per cent), and brachial (55 per cent). 

As far as the arteries of the extremities are concerned, the same partial, 
quite unaccountable distribution of hypertrophic and degenerative changes 
that are met with throughout the rest of the vascular system, seems to obtain. 
In defective metabolism, however, as in diabetes, the degenerative and 
calcific varieties tend to be more intensely and diffusely present. The degree 
and site of involvement of the several arteries of a limb, too, follow no known 
laws. Sometimes we glean the impression that the popliteal, especially at 
its bifurcation, and the distal parts of the arteries and posterior tibial are 
localities of predilection, only to be surprised at their relative integrity in 
other cases. 


CHAPTER LXVIII 

ARTERIOSCLEROSIS—MINUTE PATHOLOGY 

For a comprehension of the organic alterations responsible for the circula¬ 
tory affections and gangrene of arteriosclerotic nature, it will suffice to discuss 
merely those arterial lesions that are sufficiently advanced to bring about 
nutritional disturbances. And so we give but passing mention to those well- 
known early changes in which the intima alone is but slightly involved. In 
the chapter on the architecture of the normal arteries, it was pointed out 
that limited hypertrophies of the intima begin at a very early age. In Fig. 
129 a minute patch of intimal hypertrophy is well depicted in a normal 
anterior tibial vein. More pronounced are the lesions in Fig. 130, macro- 
scopically apparently “normal” external plantar artery, where thickening of 
the intima and hyalin change are easily discernible. The intermediate 
alterations from these minimal ones to the exceedingly destructive processes 
are so well known as to require no detailed description. We shall confine 
ourselves to an exposition of those personal observations on arteries dissected 
out from amputated limbs, in which the lesions were responsible for trophic 
disorders and gangrene. 

The larger arteries in arteriosclerosis are not infrequently narrowed by the 
presence of a glassy gelatinous-like tissue of bluish pearly and yellowish 
appearance, arising from the inner wall of the vessel. 

On section through such arteries this is seen to be made up of altered clot, 
or of proliferated intima with secondary degenerative changes. In thrombo¬ 
angiitis obliterans we rarely meet with such regressive phenomena in the 
occluding tissue, the latter being better nourished, both by reason of the 
number of vascular elements, and also because the nutritional conditions are 
far better in vessels of younger people. 

Characteristic of the disease of the larger arteries is the production of a 
layer of new-formed tissue (crescentic on cross section), poor in capillaries and 
rich in hyalin connective tissue. Two types are met with; one in which the 


ARTERIOSCLEROSIS—MINUTE PATHOLOGY 


403 


cells are abundant and in microscopic sections give the tissue an appearance 
simulating unaltered young cartilage; and another form, in which the active 
tissue shows small compressed spaces containing distorted fixed or endothelial 
cells, pigment and degenerate nuclei. In such tissues as these, by reason of a 
sort of myxomatous degeneration, a gelatinous macroscopic product is elabor- 



Fig. 129.—A portion of a normal anterior tibial vein showing a small focus of hypertrophy 

of the intima ( x ). 

ated. Near the media, vascular spaces are frequently formed, lined with 
endothelium, these being the dilated remnants of new-formed vessels that 
have penetrated and vascularized the tissues. In addition to the previously 
mentioned regressive changes fatty degeneration and atheroma also take place. 

Organized clot also may contribute to the formation of the glassy gela¬ 
tinous looking material seen in such arteries. The clot becomes organized 
in typical fashion; with this process penetration with new-formed vessels and 


404 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


proliferation of capillaries takes place. Later degeneration of myxomatous 
and hyalin variety sets in. 

The obliterative lesions and the vascular lesions are well shown in Figs. 131 
and 132 where the popliteal artery is the seat of typical atherosclerotic lesions 
with some calcification and complete occlusion, atheromatous material and 
intimal thickening. A reference to Fig. 131 will make clear the usual type of 
reduplication of the internal elastica, and the extent of.the thickening of the 
intima, and will also show a recently organized clot whose architecture is 
totally different from that of thrombo-angiitis obliterans. 



Fig. 130.—“Normal” external plantar artery with but slight hypertrophy of the intima 
(a); early lesions of atherosclerosis. 


The paucity of lesions in the adventitia is diagnostic for arteriosclerosis. 
There is no cellular infiltration, no thickening and no adhesion between it and 
the surrounding structures. 

In the media the inflammatory and productive lesions of thrombo-angiitis 
obliterans are absent, but characteristic are the lime deposits and the degener¬ 
ation of the musculature. In Fig. 133 elastic tissue stains show clearly that 
the normal course of the circular elastic fibres is interrupted by lime deposits, 
atheroma, and even bone formation. 

The enormous thickening of the intima with the formation of character¬ 
istic plaques is seen in Fig. 132 ( b ). Here there is a concomitant production 
of elastic elements, the tissue having no relation to the clot, but being the 
product of a proliferative process. This in places shows the typical degenera¬ 
tive phenomena—cellular and connective tissue degeneration with atheroma. 



ARTER1 OSCLEROSIS—MINUTE PA THOLOGY 


405 





Fig. 13i.—T he difference in healing properties of the hypertrophied intima detached 
above (at h ) and the organized clot can be appreciated in the greater darkness of the former; 
the loss of tinctorial properties of the degenerate intima at c as compared with the portion at 
b is well shown. At h the hypertrophic intima between h and the dotted line e-f has been 
detached artificially, and fuses in the picture with the organized clot. 



406 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 132.—High power of the region b and c of the artery previously shown; at b the 
markedly hypertrophied intima; at c undergoing myxomatous degeneration, the clot 
probably beginning at this point where it is adherent at j. 




ARTERIOSCLEROSIS—MINUTE PATHOLOGY 


407 


The obturating tissue depicted in the figures will demonstrate the differ¬ 
ences between the occluding tissue characteristic of arteriosclerosis and that of 
thrombo-angiitis obliterans, and that the obturating tissue, as here exempli¬ 
fied, is composed of degenerative hyalin or myxomatous fibrillar variety 
in which the vascular elements are scarce or absent, plus the fused partly 
organized, partly degenerate thrombus. 



Fig. 133.—Cross section of a plantar artery in a case of arteriosclerotic gangrene. 


The Larger Arteries in Gangrene. The Obliterating Tissue. It is not 
always easy to distinguish microscopically between organized thrombus and 
arteriosclerotic proliferating tissue, both of which may partly or completely 
occlude the arterial lumen. The pearly, glassy or whitish tissue that com¬ 
pletely fills such a lumen in atherosclerosis is most often the hyperplastic 
intima in a state of hyaline degeneration. The production of a peculiar 
hyaline tissue in which there is a rather sparse distribution of fusiform or 
stellate compressed cells is a characteristic feature of the obturating tissue 
(Figs. 134 and 135). This type of picture offers a noteworthy point of 
differentiation between the sclerotic connective tissue of thrombo-angiitis 


408 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 134— Occlusion in arteriosclerosis. The artery in the picture is closed by fibrotic 
tissue which is poor in cells and shows hyaline degeneration, as well as two foci of bone 
formation. These are seen in the dark areas, which, on magnification, would show bone 
cells and lime deposits. Here, too, the characteristic collections of mononuclear cells in 
the media without any inflammatory process in the adventitia is pathognomonic and per¬ 
mitting of differentiation from thrombo-angiitis obliterans. The absence of fusion of 
artery and vein distinguishes this from the advanced periarteritis of thrombo-angiitis. 


ARTERIOSCLEROSIS—MINUTE PATHOLOGY 


409 


obliterans and that of atherosclerosis. For the most part its lamellae or 
pseudo-lamellae (since these are merely separated by cells) are disposed more 
or less concentrically, but variations occur. Their course may be longi¬ 
tudinal, and cross sections of bundles are thereby obtained. It is, however, 
in the neighborhood of canalizing vessels that a distinct interruption of the 
general monotony of this picture is produced, for here the connective tissue 



Fig. 135. —Completely obliterated dorsalis pedis artery (part of cross section) in a case 
of atherosclerosis with diabetes and gangrene. Lumen completely filled with character¬ 
istic proliferative intima, fibers of which run longitudinally or roughly concentrically; 
below, lime deposits and bone formation just under the internal elastic lamina; above, and 
elsewhere in the media perivascular and intermuscular collection of round cells; dilated 
capillaries, spaces, and sinuses in the media (high power of a part of Fig. 134). 

fibers are often disposed in longitudinal fashion about the new-formed vessels, 
so that larger and smaller punctuate areas representing fibers transversely 
cut distinctly modify the general tone of the picture (Fig. 135). 

Often the lumen is filled with connective tissue of less dense structure, 
containing pigment, whenever organization of a clot has taken place. Thus 
pictures resembling the old obliterative process of thrombo-angiitis may be 



410 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 136. —Complete occlusion through organizing connective tissue of an athero¬ 
sclerotic artery; areas of calcification along the internal elastic membrane, thickening of the 
intima, loose connective tissue occupying the lumen. 



ARTERIOSCLEROSIS—MIXUTE PA THOLOGY 


411 


produced (Figs. 136 and 137). The intensive elastic tissue production 
sometimes seen in arteriosclerosis is well shown in Fig. 138. 

Recent Occlusion of Atherosclerotic Popliteal Artery— The clinical 
manifestations of sudden occlusion of the popliteal artery as a complication 
sometimes precipitating gangrene are described elsewhere (Chap. LXIX). 
Mechanical or stagnation thrombi are not uncommon in arteries that are 
more or less stenosed and partly occluded by hypertrophic intima. The 
intima usually has undergone considerable hyaline or myxomatous change 



Fig. 137.—Low power of the completely occluded dorsalis .pedis artery in a case of 
arteriosclerosis. The lumen is filled with organized thrombus and large new-formed 
vessels. The media above shows infiltration with mononuclears and numerous lime 
deposits in places. The intima is thickened in typical fashion. 


with secondary atheromatous and lime deposits. Cholesterin and foreign 
body giant cells are not infrequently seen. The media also shows regressive 
changes, and in addition is characterized in the longitudinal sections of the 
arteries by the presence of numerous dilated vessel spaces, that doubtlessly 
represent an intramural collateral circulation, if such a term may be employed 
in this sense. A reference to Figs. 139 and 140 will show recent thrombosis 
in the popliteal artery. In Fig. 139 a cross section shows complete occlu¬ 
sion by clot; and Fig. 140 shows a longitudinal section of the popliteal 
artery, with distal termination of the clot. 

The Media in the Obliterated Arteries. —For purposes of differentiating 
this disease from thrombo-angiitis obliterans, some knowledge as to the 
picture presented by the media at various stages of the atherosclerotic and 
obliterated process should be well understood. The changes are degenera- 



412 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 



Fig. 138. —Arteriosclerotic lesion in a vein and artery. The typical proliferation of 
elastica in arteriosclerosis is shown, as well as the splitting of the internal elastic laminae. 
The absence of perivascular inflammation is also seen, and the large vein shows marked 
endophlebitis, the intima being markedly thickened so as to occlude about one-third of 
the lumen. 



ARTERIOSCLEROSIS—MINUTE PA THOLOGY 


413 


tion of muscle, and at the boundary between the media and intima, atrophy, 
disappearance of muscular elements, calcification, bone formation, cellular 
infiltration and vascularization. 

Media Lesions when the Lumen is Filled .—When the media itself is free 
of lime deposit or larger degenerative processes and fatty deposits, the 
reactive responses due to the changes within the lumen find their best expres¬ 
sion. The striking alterations are the areas of cellular infiltrations and the 
new-formed vessels. 



Fig. 139. —Recent thrombotic occlusion of the popliteal artery. The media shows 
bone formation, calcification and the usual regressive changes; so also the typical hyper¬ 
trophic and degenerative changes are present in the intima. 


Just under the internal elastic lamina, we sometimes see collections of small 
round cells that often have a perivascular distribution in that a small capil¬ 
lary or arteriole is found within their midst (Figs. 134 and 135)* Such foci 
can be traced extending in rows of cells between the more centrally placed 
muscle fibers of the media, and separating these considerably. Often such 
areas correspond to rather extensive infiltration of similar nature throughout 
the central half or more of the muscular layer, where longitudinally or 
obliquely penetrating capillaries also invade the media. In general the 
appearances here described are those of small foci of lymphoid cells. 

In addition there may be an increased number of migrating cells scattered 
here and there throughout the middle coat. The vascular changes in the 
media are prone to strike the eye as unusual. An abnormally large number 




414 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


of capillaries or even sinuses occupies the central layers of the media, some 
traceable for a considerable distance in a circular direction, others found to 
connect with vessels traversing obliquely through the media and into the 
adventitia; and still others, in direct communication with blood sinuses of 
varying size just under the internal elastic coat. The varying sizes of these 
capillaries and the sinuses with which they communicate give the impression 
that a virtual canalization or collateral circulation through the walls of the 
vessels as well as into the obturating tissue can and does occur (Fig. 135). 



Fig. 140. —Longitudinal section of the popliteal artery recently occluded (same as 
Fig. 139)- The media shows numerous dilated vessel spaces (intramural collateral 
circulation); the intima is markedly thickened, showing degeneration, atheroma. The 
lumen is filled with recent clot terminating distally (below in the picture). 


Although an increased vascularity of the media is not pathognomonic for 
arteriosclerotic processes and is present also in thrombo-angiitis obliterans, 
we have nevertheless, here a distinctive point of differentiation. For, the 
larger sinuses and the apparent attempts to form devious vascular surrogates 
for the lost lumen are wholly absent in thrombo-angiitis obliterans. 

Because of the convoluted course of the internal elastic coat and the 
marked intrusion of the plicae towards the lumen of the vessel, sclerotic 
and obturated vessels often give a picture that is confusing. For, when 
foci of special character lie in the peninsular projections of the internal coat, 
they may project so far into the obturating mass, as to appear to lie within 
the latter. In truth, on closer observation we will notice that the calcific 
deposits, the degenerate areas and the bone formation sometimes present. 


ARTERIOSCLEROSIS—MINUTE PA THOLOGI 


415 


are confined to the media or lie in such prolongations. Arteries that show 
small areas of lime deposit in the internal coat, in and just outside of the 
internal elastic lamina, may often give the appearance of lime plaques within 
the occluding mass. However, one sees just at the internal limiting mem¬ 
brane a larger or smaller focus of lime deposition, often partially converted 
into bone or osteoid tissue (Fig. 135). It is significant, too, that immediately 
adjacent to, or leading up to such areas, we almost always find one or more 
minute vessels. 



1 

L 


Fig. 141.—Cross section of occluded popliteal artery in atherosclerosis (same as Fig. 
131). The greater part of the lumen, were it not for the artificial retraction of the obturat¬ 
ing mass would be filled except for the roughly elliptical area of lumen left at a. The 
obturating tissue is composed of hypertrophied intima most marked at b, myxomatous at c, 
making a crescentic zone of firm, partly degenerate tissue. The rest of the lumen is filled 
by organized clot, also in state of degeneration (hyaline, myxomatous) fusing imper¬ 
ceptibly with degenerate intima, but distinguishable from it by the absence of elastic 
tissue. At a residual lumen; at b typical intima proliferation; at c hyaline or myxomatous 
degeneration of intima; d to e to/ to g represents organized somewhat degenerate clot, fusing 
intimately with the detached intima along the line ef . 

Arteriosclerosis with Mixed Occlusion. —The occlusive process may be 
wholly due to the thickened intima and the heaping up of degenerative 
products. On the other hand, to the crescentic shaped 1 hypertrophy of a 

1 On cross section. 


416 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


part of the wall of the intima, occlusive thrombosis may be added, and the 
end-products after organization, develop into a tissue of varying appearance 
and consistency. Sometimes it may be glassy, gelatinous, pale, greyish-white 
or yellowish in appearance, or possess an admixture of red areas of recent 
clot; or it may contain brownish firm clots that represent earlier stages 
of organization. We often find the peculiar gelatinous tissue in the larger 
arteries, such as the popliteal. 

A study of most of the atherosclerotic lesions and of the occlusive throm¬ 
bosis may be made from Figs. 131 and 141, taken from a popliteal artery 
in a case of gangrene. 

The media and adventitia show the usual characteristic changes of arterio¬ 
sclerosis. In the adventitia the striking features are the absence of inflamma¬ 
tory lesions and of perivascular fibrosis (the latter so characteristic of 
thrombo-angiitis). 

Even a gross view of the middle coat reveals a noteworthy disorganization, 
in the varying thickness and the degenerative products. While in places it is 
very thin, in others the normal girth is well conserved or increased. 

In those portions of the media in which but little attenuation has taken 
place, the nature of the process is most easily demonstrated in arteries of this 
sort. The degeneration of the muscle fibers, their separation by infiltrating 
fatty deposition, and minute granules of lime in streaks or in plaques are the 
significant changes. These are so well known as to require but passing men¬ 
tion. However, it should be borne in mind that the infiltration with lime 
deposit goes on so insidiously that large areas are already extensively involved 
before the calcareous plaques are definitely formed. 

The Occluding Tissue.—As above stated this is composed of two distinct 
portions which may fuse so imperceptibly as to be microscopically indis¬ 
tinguishable except on close scrutiny, namely, the crescentic and partly annu¬ 
lar intimal hypertrophy in its varying aspects of degeneration and the 
organized clot. A reference to Figs. 131 and 132 will make clear how difficult 
it may be except with a high power objective to clearly separate the hyalin 
(or myxomatous) hypertrophied intima from the organized clot that has 
undergone a similar regressive process. 

A reference to Fig. 131, which is stained with the elastic tissue stain, 
however, clearly shows that even the degenerative intima takes on a suffi¬ 
ciency of this stain (orcein) to demonstrate its greater age, and the concentric 
and more or less parallel arrangement of the elastic fibrils therein. 

The Intima in the Larger Vessels. —Sufficient emphasis has been laid upon 
the nature of these lesions in the text books to make a detailed description 
superfluous here. We shall, therefore, dwell only upon those minutiae that 
may be important for those who wish to study the relationship of the throm¬ 
botic lesion in these vessels and those in other vascular affections; and those 
changes shall receive attention which are at first sight confusing and difficult 
of recognition and differentiation from the hyalin degenerative alterations 
occurring in bland organizing thrombosis. 

Much can be learned from a study of those larger arteries in which the 
pulsative and distensive stresses find their most intensively elaborated reac¬ 
tion in hyperplasia, as in the popliteal and femoral arteries. 

The typical tissue with its peculiar cell inclusion of a hyalin nature, so 
characteristic of intimal thickening forms plaques of varying size, that intrude 
into the lumen and bring about a corresponding coarctation. While the 
nature of this tissue is easily recognizable under the microscope, certain 
portions of it, when undergoing degeneration (Fig. 132), and when the fibers 


ARTERIOSCLEROSIS—MINUTE PA THOLOGY 


417 


are separated by fluid infiltration, may so closely resemble the hyaline 
degeneration of organizing blood clots, that confusion may arise. 

Elastic tissue stains, however, give the most reliable information and 
permit of the best differentiation between a clot and the degenerate intima. 
Grossly, such separation is not always possible. 

If we refer to the figures, such as Fig. 132, in which the elastic fibers of the 
intima are brought into view, three distinctive forms are encountered; 
firstly, duplication of the internal elastic lamellae; secondly, the old concentric 
proliferation of new elastic tissues in the hypertrophied intima; and thirdly, 
those sparse and irregularly disposed elastic fibers that are found in the regions 
of the intima that have undergone degeneration. 

A reference to Figs. 132,138 and 142 will illustrate clearly the nature of the 
reduplication of the internal elastic lamina in typical fashion. 

In the second zone (Fig. 132 at b ) clearly brought into view by the stain 
the elastic fibers are distinguished by that lack of continuity that has been 
previously referred to (Fig. 131). They are detached short fibrils, deposited 
in the intercellular substance, and therefore surround and embrace the 
characteristic cellular inclusions. From the intensity of the stain, however, 
we can adjudge that they are of considerable age, and their general conforma¬ 
tion and interrelationship stamp them at once as a part of a new-formed 
intima wholly separate from the organized clot. 

The third zone (Fig. 132 at c ) may be single or multiple and comprises 
that portion of the intima which has undergone degeneration. A lenticular 
area of this hypertrophic intima is apparently of different structure, in that it 
stains less deeply, and has a greater affinity for the hematoxylin stain, 
also in the wide separation of the cells contained therein. In these a sort 
of hyaline or myxomatous and in part fatty degeneration takes place, with 
a consequent disruption of the few fibers of elastic tissue therein contained. 
As a result, the elastic tissue stains are much less deep, since the fibers are 
less numerous and broken up. It is these degenerative areas which, when 
fused with the organized clot, make a composite mass that might be incor¬ 
rectly interpreted as having the same origin, but which belong on the one 
hand to the intima, on the other hand to the blood clot. The absence of 
the diffusely deposited elastic fibrils in the organized clot distinguish the 
latter (Figs. 131 and 132). 

The organized clot in such vessels presents nothing unusual. However 
in those obturating masses of thrombotic origin that have undergone degener¬ 
ation, and in which surface vascularization cannot take place by reason of the 
poor circulatory conditions in the vessel wall, there is a relative preponderance 
of myxomatous or hyaline degenerate connective tissue with rather few 
organizing vessels. In places the degeneration may be of a nature similar to 
that going on in the contiguous intima, so that the two fuse into a mass whose 
identity can only be cleared up through the elastic tissue stain (Figs. 131 
and 132). 

The peculiar hyaline thrombi give important information regarding the 
differences in the response of the more muscular arteries, and of the larger 
type of arteries, to the thrombotic processes. The lack of reactionary elastic 
activity and hyperplasia in the clots of the larger vessels is in keeping with the 
vascular and more elastic nature of the arterial wall. Wherever we are deal¬ 
ing with thromboses in the smaller more muscular vessels, in which easier 
penetration with new-formed vessels from the adventitia can take place, we 
find more firm connective tissue in the clot, and more rapid organization. The 
myxomatous and hyaline clots are characteristic of the larger vessels. 

27 


418 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The Pathology of the Smaller Vessels. —By illustrative description of the 
varying lesions in the smaller vessels, much of diagnostic value can be learned, 
and the interpretation of pictures simulating thrombo-angiitis obliterans can 
be facilitated. It is when we are dealing with gangrene and in cases in which 
the vessels show but sparse distribution of atherosclerosis, and where the 
advent of gangrene seems to be attributable to extensive thrombotic closure 
of the popliteal, that the exact nature of obturating lesions in the peripheral 
vessels (plantars, dorsalis pedis, posterior tibial, etc.) may require some 
analytical skill. In the chapter on the Clinical Course of Arteriosclerosis 



Fig. 142. —Cross section of posterior tibial artery in case of atherosclerosis. The lumen 
is completely filled with new-formed tissue; to the left and above, there is a large clear area 
with fatty degeneration, with slit-like spaces containing cholesterin crystals, two of which 
(needles) can be distinctly seen at about 8 or 9 o’clock as sharp black lines; the character¬ 
istic reduplication of the elastic membrane, and the absence of periarteritis and the normal 
separation of the vein above and to the left in the picture from the artery with no inflam¬ 
matory process intervening, are well shown. 

with Thrombosis the manifestations of this combination of lesions have been 
discussed. There we have dealt with the differentiation between chronic 
atherosclerosis attended with recent popliteal or femoral thrombosis on the 
one hand, and thrombo-angiitis obliterans with engrafted thrombotic arterio¬ 
sclerosis on the other. While the recognition of bland thrombosis in the 
popliteal is easy when it complicates arteriosclerotic lesions, some of the 
older isolated obturating foci in the peripheral vessels may be more difficult 
of interpretation. 

Although old canalized thrombi in arteriosclerotic vessels occasionally 
give pictures almost identical with thrombo-angiitis obliterans, except for 



A R TERIOSCLEROSIS—MIN U TE PA THOLOG Y 


419 


the associated calcific and degenerate changes in the walls, an investiga¬ 
tion of more material will usually reveal pictures that are distinctive of 
arteriosclerosis. 

It is the degenerative phenomena of the proliferated intima, the character 
of the internal elastic membrane and the regressive and degenerative changes 
in the subintimal layers and media that are pathognomonic for arterio¬ 
sclerosis. And so, whenever a large part of the obturating tissue shows these 
characteristics, the diagnosis of arteriosclerosis can hardly remain in doubt. 
In thrombo-angiitis obliterans fatty degeneration does not take place in the 
obturating tissue. 



Fig. 143.—Cross section of artery of the leg in a case of arteriosclerotic and diabetic 
gangrene. The lumen is almost closed by onion-like concentrically and eccentrically 
placed proliferation of the intima, the larger ovoid space being the narrowed lumen, the 
longer narrower spaces being artefacts. The lime deposit in the intima, the nature of the 
intimal proliferation, and the absence of vascularization of the media, when thrombosis is 
not present, are here well demonstrated. 


A reference to Fig. 142 will show a part of the posterior tibial artery in a 
case of atherosclerosis associated with popliteal thrombosis. 1 A large part 
of the occluding tissue here is made up of tissue in which there are a multitude 
of spaces containing cholesterin crystals. The typical retracted spaces along 
the margins of which the well known cholesterin giant cells are to be found 
in some of the sections are diagnostic of arteriosclerotic intimal degeneration. 
The associated regressive foci with lime deposits just under the reduplicated 
internal elastic laminae are also striking features. Furthermore, the absence 

1 See p. 423, Case S. S. 


420 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


of periarterial fibrosis and the lack of fusion with the practically normal 
vein, are features belonging to the same disease. 

Arteriosclerosis with Calcification. —A common type is the one illustrated 
in Fig. 143, where the distal part of the anterior tibial, at the junction of the 
dorsalis pedis depicts the ordinary concentric infringement upon the vessel 
lumen. The obturation originating from the walls is usually eccentric in 
that the mural thickening is greater at one portion than at another, giving 
the characteristic crescentic encroachment of the lumen seen upon section of 



Pig. 144. —On the right is a muscular branch of the popliteal artery with extensive 
advanced calcification and bone formation (pipe-stem artery). The pale, inner layer is the 
zone of intimal thickening with osteoid tissue and calcification on the right. The darker 
band encircling the artery represents lime deposit. To the left, an accompanying vein 
with marked thickening of the intima, hypertrophy (phlebosclerosis). 


the vessel. Such a picture would hardly give any cause for misinterpretation, 
since certain distinctive features are represented by it. The new-formed 
tissue shows a paucity of cells, the peculiar diffuse degeneration, and the 
deposit of lime. The last is more intense near the internal elastic lamina. 
The absence of periarterial fibrosis is also well illustrated here. 

When the calcareous deposits are extensive—and these may affect the 
very smallest branches as well as the large—the well known pipe-stem arteries 
are formed. The process is well illustrated in Fig. 144 where the accompany¬ 
ing vein is the seat of marked intimal thickening (phlebosclerosis), and 
hypertrophy. 



ARTERIOSCLEROSIS WITH THROMBOSIS—CLINICAL COURSE 421 


An even more striking picture is that presented by those specimens where 
there are large plaques of lime deposit and bone formation (Fig. 133 at 12 
o’clock). The lenticular or crescentic hyperplasia of the intima is beautifully 
shown. 

Bone Formation in Sclerotic Arteries .—This process is so well known, that 
but a few characteristic pictures need be shown here. These will demonstrate 
the cellular activity that accompanies both the resorption of the lime, and 
the conversion of connective tissue and lime into osteoid and osseous tissue 
(Buerger and Oppenheimer 1 ). The action of cells similar to those known^as 
osteoblasts and the conversion of lime areas into bone are well shown in 
Figs. 133 and 145. 



Fig. 145.—A small portion of the media of an atherosclerotic artery in which bone 
formation is depicted; above, the fibres of the media infiltrated with small round cells are 
seen; in the middle the dark area represents calcified material in which bone formation is 
going on; the central portion has been replaced by connective tissue containing small 
vessels and numerous round cells; the areas of bone formation are well depicted. 


CHAPTER LXIX 

ARTERIOSCLEROSIS WITH THROMBOSIS—CLINICAL COURSE 

Arteriosclerotic Gangrene with Thrombosis. —Sudden thrombosis or 
extension of old thrombotic process in arteriosclerosis must be regarded 
as being a complication of extensive arteriosclerotic or atherosclerotic 
disease of the vessels of the lower extremities. If we study the pathological 
findings in the arteries of legs amputated for gangrene, and compare these 
1 Buerger and Oppenheimer, Jour. Exper. Med., April, 1908, Vol. X, 3. 


422 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


with the clinical history, we will note the following causes for gangrene in 
athero- and arteriosclerosis: first, that the circulatory inadequacy or insuffi¬ 
ciency is partly due to the loss of elasticity in the vessels, partly to concentric 
diminution of the lumina of the vessels through atheroma, thickening of the 
intima, and calcification; second, that these stages are not sufficient to account 
for the sudden advent of gangrene in some cases, nor can other sources, such 
as cardiac weakness and trauma alone, be considered sufficient as immediate 
causes. But, there is a distinct pathological explanation in the occlusion 
produced by sudden thrombus formation. This usually occurs in the popli¬ 
teal artery and extends upward into the femoral, more frequently passing 
downward into the posterior tibial artery. Histological examination of the 
femoral, popliteal and posterior tibial arteries in such cases, has demonstrated 
conclusively the importance of the role of thrombosis in the causation of the 
gangrene, the thrombus being discovered in various stages of organization, 
depending upon its age, that is, upon the time that has elapsed between the 
onset of its formation and the time of amputation of the limb. 

Clinical History.—There is usually a previous history in elderly individuals 
(over forty-five years of age) of intermittent claudication or indefinite pains in 
the lower extremities, particularly in one limb. Suddenly, the patient will 
develop the following symptoms: trophic disturbances terminating in gan¬ 
grene of small extent (one toe or more); or dry gangrene of a toe or toes, the 
foot, or portion of a leg; or, extensive dry or moist gangrene. In other Cases 
the signs of sudden impairment of circulation due to thrombosis of the pop¬ 
liteal or femoral arteries make themselves manifest without the development of 
ulcer or gangrene. These are sudden pain in the calf of the leg or foot, attended 
with paresthesiae, coldness, pallor and weakness of the limb. Examination 
reveals absence of pulsation in the dorsalis pedis, posterior tibial, possibly also 
in the popliteal arteries, pallor of the foot, slight erythromelia on depression 
of the limb, at times thrombosed veins, particularly the external saphenous. 
Hemorrhagic areas and cyanotic patches suggestive of impending gangrene 
may also appear. Improvement in circulation may then take place, so that 
the limb gradually becomes warm, the pallor and cyanosis disappear, a 
state of chronic erythromelia (rubor) being usually the manifestation of 
improved circulatory conditions. Sooner or later, however, even such cases 
may have fresh attacks of thrombosis leading to gangrene. 

A study of the vessels in such cases has shown either recent organizing 
thrombi in the popliteal artery, or, a combination of these clots with old 
organized clots, the recent thrombosis extending for a variable distance 
downward into the posterior tibial artery. From the observations on the 
conditions of the arteries, it seems that extensive obturation due to athero¬ 
sclerosis, atheroma, etc., and old thrombosis in the popliteal artery may be 
compatible with fairly good circulation of the limb. But, when an additional 
extensive recent thrombosis takes place, or, when extraneous causes (cold, cardiac 
weakness, etc.) are added, the limb succumbs to the mortifying process. 

Whilst certain patients offer a history that suggests clearly the occurrence 
of a fresh accession of thrombus formation, there are others in whom there is 
merely the story of a trophic lesion apparently precipitated by cutting a nail 
with injury to the nail-bed or surrounding skin, or by an operation for ingrow¬ 
ing nail. When an ulcer thus formed is suddenly complicated by a turn for 
the worse, with more deficiency of local circulation, it is usually due to recent 
thromboses in the popliteal or posterior tibial arteries. 

After pain in a toe (usually the big toe) for a variable time, a period of 
intermittent claudication, a trauma, or without cause, an ulcer forms and 


ARTERIOSCLEROSIS WITH THROMBOSIS—CLINICAL COURSE 423 


refuses to heal. There is gradually deepening cyanosis and coldness about the 
affected region. Erythromelia, and ischemia can be elicited and the pulses 
up to the femoral are usually absent. Suddenly the toe begins to look black 
and the foot becomes colder, gangrene being imminent (recent thrombosis?). 
Even such cases may respond and heal under the postural method . 1 

Bland thromboses are apt to occur in the popliteal or upper posterior 
tibial artery with extensive gangrene of sudden advent as a sequence. The 
lesions of thrombo-angiitis obliterans, too, may have preceded with partici¬ 
pation of*some of the peripheral vessels, such as the dorsalis pedis and 
plantars. When alterations in the latter are of very long standing and second¬ 
ary degenerative changes (calcification) coexist, a clinical differentiation 
from arteriosclerosis may be no longer possible. The cases allow of the follow¬ 
ing grouping: 

(1) Advanced atherosclerotic diffuse processes, thrombotic occlusion and 
organization in the peripheral vessels with superadded recent bland throm¬ 
bosis leading to gangrene of sudden onset. 

(2) Advanced atherosclerotic diffuse processes, old thrombo-angiitis 
obliterans of limited extent in the peripheral vessels, recent bland thrombosis 


and gangrene. e . 

An excellent example with thrombosis of the popliteal artery is the 

following: 

S. S., male, age 59 years, had intermittent claudication and cramp-like pain in the right 
leg on walking, dating back 4 months. Six days before he reported for examination, an 
ulcer appeared over the right big toe, which increased gradually in size without much pain. 
Two days thereafter the toe became black, and the patient suffered repeated chills. He had 
noticed redness, tenderness and swelling of the right leg the following day. He had no other 

7 Physical examination (author’s notes taken January 30, 1915) showed the big toe of 
the right foot to be bluish and livid, and evidently the seat of rather extensive gangrene, 
the cyanotic color being rather deep, the toe cold. At its root the skin was very deep blue, 
blackish and in the early stages of gangrene. The color was apparently altered by reason 
of the detachment of the epidermis and a collection of fluid (serum and blood) underneath 
if in short, a large blackish bleb of irregular contour. A bulla was also noted over the 
second toe which was almost completely black. The third toe was also cyanotic. The 
fourth toe showed several black blebs, and the fifth toe a very large bleb of similar nature. 
The dorsum of the foot showed the changes above described oveqthe toes, the greater part 
being reddish because of an inflammatory process. The usual evidences of rapidly spread¬ 
ing moist gangrene of the foot developed. Running upward along the internal saphenous 
vein and well into the saphenous opening, there was a strand of lymphangitis. 

On elevation of the foot pallor ensued, particularly at the roots of the toes where this 
was very marked in contrast to the very bluish discoloration of the gangrene. The dorsalis 
pedis, posterior tibial and popliteal pulses were absent, the femoral present. 

A section of the limb amputated through the lower thigh, January 30, 1915, was exam¬ 
ined January 31, 1915, and showed the following conditions, as recorded in the protocol: 

The Gangrene— The blackish bullae contain sanguinous fluid, reddish, some with dark 
blood, others with light, and some with serum and blood. On cutting the skin we find that 
the bluish discoloration penetrates for varying distances, 1 mm. or more. Along the course 
of the internal saphenous vein, there is evidently lymphatic infection, for pus can be 

squeezed out of the lymphatics. . ,, , . .. 

The Vessels. —The popliteal artery at the site of amputation just above the knee in its 
lower fourth, contains fairly firm organized clots with marked atherosclerosis of the vessels, 
a sort of glassy or gelatinous clot such as we get in atherosclerosis with secondary thrombo¬ 
sis. As the artery is traced downward, the clot becomes more red , finally terminating m a very 
recent red clot just above the bifurcation of this vessel. It is apparent that there was an old 
thrombotic process followed by recent extension of the clot (tail portion). Below this, the 
posterior tibial artery simply shows the lesion of atherosclerosis, as does also the peroneal, 
but without thrombosis. In the lowermost parts of the posterior tibial artery are some 
dosed areas that may either be due to an old thrombo-angiitis obliterans plus arteriosclerosis 


1 See Chap. LXV, p. 380. 


424 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


and thrombosis, or simply arteriosclerosis plus thrombosis. The anterior tibial in its upper 
half is patent and shows the lesions of arteriosclerosis. The lowermost portion is closed 
he *e and there. Macroscopically differentiation is impossible between an arteriosclerosis 
plus thrombosis or thrombo-angiitis obliterans. From a clinical standpoint, the features 
of arteriosclerotic gangrene were here presented. The absence of an old history of thrombo¬ 
angiitis obliterans, the age of the patient, the rather short duration of the symptoms, of 
intermittent claudication, the wet type of gangrene, the. bullae, the diffuse infection 
and lymphangitis, all these were rather suggestive of arteriosclerosis. However., an old 
thrombo-angiitis obliterans of limited extent in a latent or cured stage with superimposed 
arteriosclerosis and secondary thrombosis of the popliteal artery could have produced a 
similar outcome. 

Such sudden gangrene and lymphangitis are usually encountered where 
rather extensive thrombosis takes place in larger arteries , a lesion superimposed 
upon an old occlusive process in other territories. Such vascular occlusion can 
be clinically interpreted in the light of two possibilities: (i) thrombo-angiitis 
obliterans with secondary degeneration or atherosclerosis followed by bland 
thrombosis in previously patent arteries; and (2) arterial disease of the arterio¬ 
sclerotic type with here and there areas of bland thrombosis secondary to the 
arteriosclerotic process. 

In several instances of the above type of clinical history and arterial lesions 
with gangrene, data could be obtained to warrant the following conclusions. 

Conclusions. —(1) In some cases we seem to be dealing with arteriosclerotic 
changes, popliteal obturation through old thrombosis, with recent extension 
of the thrombus downward to the bifurcation of that vessel. 

(2) Marked infection of recent advent follows, thrombotic gangrene of 
considerable areas, and extensive lymphangitis. 

(3) In elderly people it is difficult even at autopsy of the limb to determine 
with certainty as to whether there exists one of the following: simple arterio¬ 
sclerosis with thrombosis; or thrombo-angiitis obliterans in peripheral vessels 
upon which is engrafted a secondary arteriosclerosis and a subsequent recent 
accession of thrombosis. 

Arteriosclerosis with Thrombosis of the Larger, More Central Paths. —It 

is most difficult to differentiate between embolic gangrene, particularly of the 
lower extremity, and thrombotic processes, when gangrene is of sudden advent 
and complicates intensive athero- and arteriosclerosis, especially in diabetes. 
We are called to see a patient usually over 40 years of age, who gives a history 
of having had a bad heart, some evidences of arteriosclerosis with or without 
diabetes. Suddenly there is pain in the calf of the leg, in the foot or the 
knee, the limb becomes powerless and cold, and gangrene rapidly sets in, the 
extremity below the knee, or even up to the upper fourth of the thigh showing 
the usual signs of imminent gangrene. None of the pulses below Poupart’s 
ligament are detectable. 

At amputation through the upper fourth or upper fifth of the thigh, the 
femoral artery and vein are found closed with recent red blood clots, and there 
is very little or no bleeding. But the artery shows intensive atherosclerosis 
and its lumen is reduced to less than half of the normal. 

So, also, is it hard to distinguish between an embolism of the external 
iliac or common iliac, and thrombotic occlusion superimposed upon 
intensive atherosclerosis, a lesion not infrequently seen in the popliteal artery. 
Wherever the condition of the heart warrants the diagnosis of cardiac 
thrombi, and whenever the future course of the malady demonstrates that 
emboli are being cast off from time to time into other territories, the embolic 
nature would seem to be established. In the absence, however, of such a 
course and such cardiac signs, we may be dealing with a thrombotic process 
superadded upon intensive atherosclerosis. 


ARTERIOSCLEROSIS WITH THROMBOSIS—CLINICAL COURSE 425 

Although the more usual lesions leading to gangrene due to extensive 
occlusion and thrombosis in the peripheral territories are below the knee and 
at the popliteal, an acute advent of thrombosis or embolism in the external 
iliac or upper femoral arteries is occasionally seen. In these cases the gan¬ 
grene is of sudden advent, extensive, and gives the picture of the embolic type 
described under embolic gangrene. The femoral artery may be found patent 
up to within one or two inches of its origin, where a tail clot of a femoral clot 
higher up is encountered. The following brief history will elucidate. 

B. H., female, age 67, arteriosclerotic, gives a history of the sudden advent of coldness 
of the right foot and leg, 10 days ago, without abdominal pain or cardiac distress. Immedi¬ 
ately thereupon all the signs of dry gangrene made their appearance. 

Upon physical examination well advanced gangrene of the right foot is seen; cyanosis 
to the upper fourth. The thigh is warm to the lower third. 

February 12, 1923, circular amputation through the upper fifth; very little bleeding 
although no tourniquet applied. The femoral artery does not pulsate, and on section 
a red clot, representing doubtlessly the tail clot of a primary clot higher up, was removed. 
The saphenous vein in the uppermost part is thrombosed. All the large veins are distended. 
The femoral artery is atherosclerotic, dilated, and eroded. 

Conclusions. —The primary clot, therefore, must have been situated above 
the point of ablation somewhere in the external iliac or most proximal part of 
the femoral artery. 

Atrophy as a Sequel. — Pseudo phthisis of the foot and leg or atrophy 
(of vascular origin) is a chronic condition not infrequently the outcome of 
thrombosis of the popliteal or of the other peripheral vessels, superimposed 
upon nutritive disturbances already the result of arteriosclerotic vascular 
disease. 

In a patient with evidences of diseased arteries, either objectively demon¬ 
strable or subjectively manifested by such symptoms as intermittent claudi¬ 
cation, the following sequence of events may occur 1st, an attack of 
thrombosis; 2nd, abatement of the acute symptoms with or without appear¬ 
ance of trophic disorders; 3rd, a condition of chronic withering or atrophy 
(for which the author suggests the name pseudophthisis or vascular atrophy) 
or, in lieu of this, gangrene; and 4th, eventually gangrene following the 
previous period after an interval of months or years. In rare instances the 
condition may develop insidiously without any history of an acute attack of 
thrombosis. 

Clinical Course .—With numerous variations but to a certain extent con¬ 
forming to the type exhibited by the case next cited this condition is trace¬ 
able to an “attack of thrombosis” with the following symptoms: sudden 
pain in the calf or in the foot, inability to walk, with pallor of the forepart 
of the foot, coldness, marked blanching on elevation, the dorsalis pedis, 
posterior tibial and popliteal pulseless, while the vessels of the other leg are 
pulsating. The blanching of several of the toes may be very marked, and 
the superficial veins, such as the external saphenous, may be palpable and 
tender. After the commencement of these symptoms, areas of gangrene 
may rapidly develop, or trophic disorders which become more striking 
when the foot hangs down; but in the absence of these, pseudophthisis or 
vascular atrophy gradually ensues. 

Acute attack of popliteal thrombosis in arteriosclerosis, subsidence of threatening gangrene, 
development of chronic atrophy of leg, semi-invalidism for two and one-half years eventuating 
in gangrene, amputation, recovery. ....... , ,, , 

S. K., male, aged 65 years, a diabetic thought he was attacked with “lumbago 5 days 
previously, though the chief complaint was “cramps” in both legs, particularly in the rig t. 
Early this morning (June 12, 1915) there was pain in his right leg, which seemd to get cold 
and numb, so that he could not bear his weight on it. 


426 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Physical Examination (Author’s notes June 12, 1915).—The forepart of the right foot 
shows "distinct pallor, with an increase in intensity and exten t of the blanching, when the 
foot is elevated. There is moderate rubor in the pendent position gradually giving way to 
cyanosis; the foot is cold and the dorsalis pedis, posterior tibial, and popliteal arteries do 
not pulsate whilst they are easily palpable in the other extremity. 

A hard cord occupies the lower three fourths of the course of the external saphenous vein. 

Diagnosis. —Thrombosis of the popliteal (possibly posterior tibial) artery with threaten¬ 
ing gangrene and thrombosis of the external saphenous vein in an arteriosclerotic. 

First Stage. —June 14. The color of the toes is slightly improved. When the foot is 
exposed for a short time, it becomes slightly cyanotic. In the pendent position there is a 
combination of cyanosis and rubor, and the patient complains of heaviness and pain in the 
sole. The outer border of the foot is red—this region described by the patient as having 
a “ hot poker ” applied to it. The thrombophlebitis of the external saphenous vein seems to 
have extended upward slightly. Over the mid-dorsum of the foot there is a patch of redness 
•enclosing punctate ecchymoses (foreboding of trophic lesions). These hazy lesions are 
intensified and easily discernible when the foot hangs down. On the following day the red 
area was more distinct and the hemorrhagic spots were converted into dark minute scabs. 

Treatment— Warmth, rest and Allen method for the diabetes instituted immediately; 
postural procedure on the 20th of June. ^ 

Second Stage of Subsidence with Impending Trophic Lesions. —June 24. Area on dorsum 
of foot in about the same condition; rubor in pendent position more marked. Pain in the 
limb has disappeared. 

July 1. Distinct improvement, color better, almost normal except for the rubor. 

July 25. The color of the foot is good except that the right foot is much redder than the 
left, and suggests the appearance of the leg in thrombo-angiitis obliterans when in the state 
of chronic erythromelia (chronic erythromelia in arteriosclerosis). 

August 1. Now able to bear weight on right foot for a few seconds; blanching still 
marked on elevation, general color of foot good. 

From now a gradual improvement without development of gangrene or ulcers, the 
•extremity passing from tlje second stage of abatement into the beginning of the third stage 
of chronic vascular atrophy. 

From August, 1915, to December, 1916, he has been an invalid, unable to walk, although 
now (December 1, 1916) he is able to get about with a cane. 

Condition of Right Leg. —December 1, 1916. There is marked atrophy of the foot and 
leg, chronic rubor even in the horizontal position, this extending to one third way up the leg. 
Ischemia is demonstrable upon elevation through an angle of 30°, and intensified reactionary 
rubor shown after preliminary elevation through an arc of 30° to 45 0 . The left leg shows 
very slight rubor and ischemia on elevation—evidences of arteriosclerotic occlusion of 
vessels. (Third stage of atrophy now marked.) 

March 28, 1917. Author’s notes read: For 23 months the right leg has been in a stage 
of chronic (vascular) atrophy, with constant tenderness of forepart of foot, dorsal and 
plantar regions, with chronic rubor and with outcropping of evanescent ecchymoses. 

April 26, 1917. Right foot.—Very much withered, hemorrhages numerous, some con¬ 
glomerate in thickly aggregated areas, some confluent in small patches, others discreet 
over the dorsum. The toes are tender and cannot be separated without causing pain, 
although there are no fissures. Subjectively, the foot feels cold, ankles and dorsum 
painful, and feels as if some “iron weight” were applied. 

Besides the erythromelia, there is noted a clonus or intention tremor of the foot as soon 
as it is flexed and not steadied against some object. 

November, 1917. Gradual onset of dry gangrene with involvement of the toes gradu¬ 
ally (December, 1917) extending upward (fourth stage of gangrene). 

December 31, 1917. Amputation by the author just above the lower third with 
excellent result. 

Pathological Examination. —The vessels showed the usual picture of marked arterio¬ 
sclerosis with thrombosis of the popliteal and upper arteries. 

Summary of the Issue after Thrombosis. —There may be frequent 

attacks of thrombosis over various territories with the following sequences: 

(1) When sufficiently extensive, thrombosis may lead to immediate 
gangrene. 

(2) It may cause merely trophic disturbances. 

(3) It may give rise to the clinical picture of an “attack of thrombosis.’’ 

(4) It may lead to mere atrophy (chronic vascular atrophy), or pseudo¬ 
phthisis of the limb; or, 


ARTERIOSCLEROTIC GANGRENE WITH DIABETES 


427 


(5) To a slight aggravation of the existing symptoms, of which intermittent 
claudication is the most striking; or to exacerbations of pain and tenderness, 
localized and roughly in the course of some larger deep vessels of the leg. 
A reference to similar phenomena and to spontaneous paroxysms of pain 
has been made in the Chapter on Pain in Thrombo-angiitis Obliterans. 


CHAPTER LXX 

ARTERIOSCLEROTIC GANGRENE WITH DIABETES 

This should not properly be classed as a distinct form of gangrene (so- 
called diabetic gangrene)* inasmuch as the pathology is the same as that of 
arteriosclerotic gangrene. The mortifying process should not be regarded as 
being due to the diabetes, but primarily as the result of extensive arterial 
obliteration. The disease may take a course somewhat different from simple 
arteriosclerosis because of the presence of the complicating diabetes. The 
symptomatology may be identical with that discussed under arteriosclerotic 
gangrene, or may be modified after trophic disorders and gangrene have 
definitely developed by reason of the hyperglycemia. 

When ulcers are present, a phlegmonous process is more apt to ensue with 
the trophic disorders as the starting point. Necrosis of the deeper tissues is 
likely to be more extensive, and moist gangrene is more frequently seen. As 
far as the changes in the arteries are concerned, these are identical with those 
of arteriosclerotic gangrene, and the calcification and atheroma are usually 
intense. 

Cases of diabetes in elderly people with fairly marked arteriosclerosis may 
present none or very few of the typical signs of impaired circulation, and still 
may develop patches of gangrene. Such gangrene usually eventuates after 
traumatism, thermal or mechanical. The development of a gangrenous patch 
over the shin bone after an abrasion, or after careless rubbing, scratching or 
massage is common. The abrasion, scratch or burn becomes converted into a 
small area of dry gangrene, involving merely the skin, rarely the subcutaneous 
areolar tissues 

On examination it will be found that blanching on elevation is absent. 
Erythromelia or reactionary erythromelia are also absent. The dorsalis 
pedis and popliteal may pulsate. The general color of the limb is good. In 
short, there are none of the usual manifestations of circulatory deficiency, 
and yet gangrene occurs. . 

These are the cases in which inadequacy of circulation is not sufficiently 
great to produce definite objective phenomena of vascular obturation in 
the peripheral parts. And still the narrowing and rigidity of the arteries, 
coupled with the presence of the metabolic deficiencies due to the diabetes, 
are sufficient to lead to gangrene of the tissues upon the mere action of a 
trifling trauma. The prognosis in these cases is usually good if treatment 
be directed toward the diabetes, if infection be prevented by giving free: exit 
to pus, when it collects under the gangrenous patches of the skin and if the 
author’s “Postural Method of Treatment” be employed together with other 

methods for enhancing the circulation. . 

Pathology— We have grouped both the arteriosclerotic and diabetic cases 
together, for the pathology of the vessels is the same. A study of the con- 


428 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


dition of the arteries and veins in limbs amputated for so-called diabetic gan¬ 
grene, reveals the fact that in each and every instance we are dealing not with 
a gangrenous process due to the diabetes per se, but a mortifying process 
dependent upon extensive arterial disease. 

In both arteriosclerotic and diabetic cases there is an extensive and intense 
athero- or arteriosclerotic process. In some cases there is marked occlusion 
due to the heaping up of atheromatous and calcific material or to a combination 
of this process and secondary thrombosis, or a moderate degree of athero¬ 
sclerosis with obturating thrombosis. These cases may be grouped under the 
caption— intense , obturating atherosclerotic process. In another series of cases 
we find that, although very few of the vessels are completely closed, the athero¬ 
sclerotic process is very extensive and intense making the vascular walls 
rigid, or producing a dilatation or pouching of the walls of many vessels. 
Both of these lesions will have as their sequence impaired nutrition of the parts, 
by virtue of the loss of elasticity in the arterial walls. This type may be 
grouped under the caption— atherosclerosis with slight or no occlusion. 

Common to both types, the diabetic and arteriosclerotic, is the fact that 
the larger veins are but moderately involved, although they may have suffered 
a moderate degree of endarteritis or thickening of the intima. 

The arterial lesions may be summed up as follows: extensive degeneration 
of the arterial walls, intense atherosclerosis, calcification, sometimes bone 
formation, often occlusion of a large part of a vessel’s course, the Arteries 
being converted into rigid pipe stems; at other times, less pronounced athero¬ 
sclerosis with dilatation of the vessel walls in places, or a combination of intense 
atherosclerosis with thrombosis. Where the latter occurs, elastic tissue 
stains show proliferation and heaping up of the elastic layers or lamellae and 
that the remnant of the lumen may be occluded by organized clot. Another 
type of lesion is that in which marked calcification of the vessel walls takes 
place, sometimes attended with bone formation. 

Complicating Infection. —The extensive phlegmonous inflammation so 
frequently seen in diabetic cases is usually associated with gangrene of 
at least the skin. Treatment is often delayed, and incisions made too late 
because the temperature may not be high at the onset, the pain only slight, 
and their external manifestations in no measure corresponding to the extent of 
the process in the depth. Whenever we meet with a small focus of infection 
in a diabetic, palpation for tenderness over the focus of the infection usually 
near the base or over one of the toes, is in order. Invasion of the plantar 
tissues and dorsum rapidly takes place, so that careful watch must be made 
from day to day for the development of tenderness along the plantar aspect of 
the foot as well as over the dorsum. In this way only can evidence of infection 
be elicited long before suggestive or external manifestations appear. As a 
rule, a consultant is called to see such cases when the phlegmonous process 
has already made considerable progress in the deeper parts although the 
surface changes may be but slight. 

Given a small focus of infection between the web of the toes, near the base 
of the toe or elsewhere in this region, a sloughing wound is apt to develop. 
Subsequent to this, tenderness may be elicited along the plantar aspect in a line 
leading from the point of original infection, or along the dorsum. Infection 
develops, a red area over the dorsum can be made out, and discoloration into a 
bluish or purplish hue is often seen. There may be but very little infection 
under the skin; but slight as this may be, it may suffice in these cases to com¬ 
promise the circulation of the superimposed integuments, and lead to 
gangrene. 


ARTERIOSCLEROTIC GANGRENE WITH DIABETES 


429 


But even with the development of such very evident signs of infection— 
redness, tenderness and fever—a clinician is apt to underestimate the extent 
of the process both under the surrounding apparently healthy skin, and into 
the depth. 

When incision is made into such areas the skin will frequently be found to be 
undermined for a considerable distance by a sloughing suppurative process, 
and the deeper tissues too. The tendons, fascia, and muscles will be seen to 
have undergone a similar destruction even though this be unsuspected. 

Diabetic Cases. —The following abstract from the author’s notes on the 
pathology of the vessels in amputated legs of cases of so-called diabetic 
gangrene will illustrate in detail the type of lesions that are found. 

I. Extensive Atheromatous and Calcific Obturation. 


P. A., April i, 1909 (diabetic gangrene): Right leg ablated at the knee joint; 
one ulcer situated at the outer border of the foot, corresponding to the. head of the fifth 
metatarsal; it is about the size of a dime, covered with sluggish, necrotic granulations; a 
secondary ulcer, slightly larger, more superficial, found at the head of the first metatarsal, at 
the inner border of the foot. 

Popliteal artery is atheromatous at the point of ablation, possibly thickened but not 

occluded. . , 

Posterior tibial is almost completely closed by atheromatous plaques. Its middle third 
is almost completely closed by degenerate atheromatous masses; the lower third shows 
similar lesions. 

External plantar is almost completely closed by atheroma. 

Peroneal in its upper part is almost completely closed by a series of atheromatous 
plaques; throughout the remainder of its course, there are yellowish, rounded atheromatous 
plaques and diffuse atheroma. 

Anterior tibial is practically closed by the atheromatous process and calcification 

throughout its entire extent. .. ,, 

Dorsalis pedis is open; but markedly atheromatous. The veins are all open; the 
external and internal saphenous are normal. 

There is no periarteritis. 

Summary. —Ulceration and beginning gangrene in a diabetic; extensive 
atherosclerosis with occlusion of many of the arteries, the veins being open. 
A typical example of the occlusive variety of the atherosclerotic process. 

II. Atherosclerosis with Thrombosis.— As an example of somewhat less 
marked atherosclerosis, associated, however, with obliterative thrombosis, 
we have the following case: 

R. A., aged 62 years, “diabetic gangrene.” Right leg: ablation 6}4 inches above knee 
joint. The dorsum of the big toe and adjacent surface of first metatarsal bone are the seat 
of beginning gangrene that has extended almost to the head of the metatarsal bone I his 
area is covered with a brownish green discolored skin beneath which lies a pool of fluid; 
when this necrotic material is wiped away, the tendon sheath of extensor muscles of toe and 
underlying bone are exposed. The necrotic material has insinuated itself beneath and 
around the extensor tendons of the second and third toes, downward as far as the base of 
these toes, and upward as far as the head of corresponding metatarsal bones. 1 he epider¬ 
mis covering the sole is easily stripped off over the anterior three-quarters of the foot, 
exposing an irregularly quadrilateral gangrenous patch about the center of the foot. 1 e 
appearance of this patch is like that described as occurring on the dorsum. It extends 
upward between the plantar fascia and muscle groups, apparently coming into contact 
with the first and second metatarsal bones and communicating with the gangrenous area 


on the dorsum. . . . , ,, 

Femoral artery is sclerotic and brittle and, at one point near the lower end there is a 
large ulceration of the intima about 3X7 mm. Just below this there is another ulcera¬ 
tion with some undermining of the intima by extravasation of blood. The vessel itself is 
patent. The femoral vein is only slightly thickened and is patent. 

Popliteal artery is patent throughout. Its wall is much thickened and somew a 
calcareous, especially in the upper part, where there is an encircling band of calcareous 
material about 2 mm. in breadth. The intima is smooth, but there is diffuse atheroma, 
this being especially marked about the orifices of smaller branches. The accompanying 
vein is only slightly thickened and is open throughout. 


430 


CIRCULATORY AFFECTION S'OF THE EXTREMITIES 


Posterior tibial, at its origin, and for a distance of about n cm. is patent; from this 
point on, there is an obliterating thrombosis of the vessel. The occluded portion is 
contracted. The vessel, as a whole, presents only a moderate degree of sclerosis, this being 
more marked from the point of thrombosis down. 

Peroneal artery, at its origin, and for a distance of about 4 cm., presents a similar picture 
to the posterior tibial. In the rest of its course there is complete obliteration by an old, 
white, organized thrombus. The accompanying veins do not show as much thickening as 
posterior tibial, and are patent. 

Internal saphenous vein shows marked thickening of wall, so that the vessel can be 
rolled beneath the finger like a cord; it is, however, open throughout. 

Anterior tibial shows a process similar to that involving the femoral though less exten¬ 
sive. Toward the lower end there is considerable narrowing of the vessel as a whole, but 
the lumen is unimpaired. 

Summary.—Gangrene associated with arteriosclerosis and atheroma of the 
femoral vessel; extensive obliterative thrombosis and atheroma of the posterior 
tibial and peroneal arteries with thickening of the internal saphenous vein. 

Another instance of extensive arterial disease is seen in the following case. 

III. Extensive Atheroma, Thrombosis with Puriform Necrosis. —Many 
valuable clinical and pathological data are afforded by the following case of 
bilateral diabetic gangrene. 

It will illustrate: 

1st. That the antecedent history may evidence months or years of trouble 
in both limbs, first as localized trophic disorders and gangrene of very limited 
extent, involving merely superficial tissues or a whole toe, but finally more 
than two years later (in the case to be cited) eventuating in gangrene of 
first one, then the other lower extremity. 

2nd. That characteristic in the diabetic cases is the insidious destruction, 
disintegration and infection of the deeper tissues, muscles, tendons and, even 
bone, masked by the superficial parts to such a degree, that often only con¬ 
siderable experience and very careful observation will succeed in giving the 
observer a proper estimate of the degree of necrosis present. 

H. B. (May 10, 1905) male, age 52 years, diabetic for thirteen years, had the third toe 
of the right foo removed for gangrene. Two years previously a patch over dorsum of left 
foot had become gangrenous, was removed and healing took place again. In April, 1905, 
a gangrenous area developed on the sole of the left; this separated spontaneously and healed. 

In May, 1907, the left leg was amputated through the thigh because of extensive gan¬ 
grene, with recovery. 

In June, 1907, a small ulceration appeared on sole of right foot, which became dusky 
red in color. Since then the gangrene has spread. 

Local Physical. —There is a gangrenous area extending over almost entire dorsum of right 
foot from the toes to the ankle. The toes are reddened but not cyanosed. The skin over 
plantar aspect of the sole also gangrenous. The parts are very tender, feel hot and show 
inflammatory changes. 

July 30. Area of gangrene on dorsum of foot has extended in lateral directions. From 
the ankle upward to about the middle of the leg there is decreasing induration and redness. 
The sensitiveness of the part is more marked as one proceeds upward. The sole of the foot 
is swollen, cold, and in its greatest extent not painful. 

Operation July 31, 1902. Amputation above knee (right). 

August 3rd. In one hour this A. M. patient passed into comatose condition, and in spite 
of reactionary measures died. 

Gross Pathology of Extremity. —Right leg ablated five and a half inches above the knee 
joint. Middle toe removed at previous operation, same cause. Extending from inner 
margin of the sole of the foot and occupying the middle two-thirds of the inner surface 
across the dorsum and three-fourths of the outer surface of the foot, is an irregular area of 
gangrene covered with a black slough. The slough is very friable, easily removed, exposing 
the underlying necrotic tendons and intervening tissue; in places the bone is exposed. 
The adjacent skin is undermined by purulent necrotic material. The region of the ankle 
is edematous and the epidermis comes away in big patches. The lower half of the leg no 
longer shows the redness observed clinically. 


ARTERIOSCLEROSIS—DIAGNOSIS 


431 


Extending upward from the outer side of the ankle beneath the tendon of Achilles and 
along the outer part of the posterior surface of the leg there is purulent or necrotic material 
extending half way up the leg between the tendon Achilles and the deep plane of muscle. 
This purulent material is also found beneath and between the muscle and tendons of the 
deep plane, the muscles themselves showing some gangrene. On the inner side of the tibia 
between the bone and the overlying skin and on the outer surface of the leg between muscle 
and the skin there is a large area of sloughing material which does not involve underlying 
muscle but chiefly the subcutaneous tissue, extending upward half way to the knee. 

Femoral vessels show periarteritis. Both vessels patent. Femoral artery wall is 
thickened, in places calcareous, and in some places thicker than in others. The intima 
shows small patches of atheroma, especially marked transversely. The intima and sub- 
endothelial layers are thrown into many transverse ridges springing from a median, longi¬ 
tudinal ridge. Between the transverse ridges are well marked pockets or depressions. 
The vein shows considerable thickening of the wall. 

Popliteal vessels patent. The process as noted above in the femoral, namely the peri¬ 
arteritis, thickening of the vessel wall, atheroma, transverse ridges and calcareous patches 
are even more marked here. The transverse ridges require further comment as in several 
places they have elevated the intima into a constricting ring which has markedly decreased 
or stenosed the lumen at these points. The vessel above and below such a ring or stricture 
forms a somewhat dilated pouch. At the lower end of the popliteal joint above the bifurca¬ 
tion, there is a well marked plaque formation of the entire vessel wall (bone?). The vein 
shows thickening of the wall more markedly in some places than in others. 

The posterior tibial just below its bifurcation downward to its termination is completely 
occluded by an old organized thrombus. The vessel itself is very much smaller in caliber 
than normal, calcareous , and shows large amounts of periarteritis. The venae comites are 
thickened. 

The peroneal artery shows continuation of process noted above in the popliteal and 
femoral, not quite so marked as in the popliteal. The peroneal vein is somewhat thickened. 

The anterior tibial artery is like the posterior tibial atrery of very much smaller caliber 
than normal and completely occluded by an old, white thrombus. The accompanying 
veins have thickened walls. 

The dorsalis pedis artery , as far as it can be traced shows a continuation of the process 
noted in the anterior and posterior tibial. 

The vessels below the ankle could not be worked out on account of necrosis. 


CHAPTER LXXI 

ARTERIOSCLEROSIS—DIAGNOSIS 

Arteriosclerotic Cases Mimicking or Simulating Thrombo-Angiitis 
Obliterans. —When we are dealing with elderly individuals over 50 years of 
age, who show evidences of the existence of a generalized atherosclerosis or 
arteriosclerosis of the vessels of the extremities, the differential diagnosis from 
thrombo-angiitis obliterans may be difficult. The cases observed by the 
author have been numerous, but a mere indication of some of the types can 
be mentioned here. The histological pictures have proven beyond per- 
adventure (Fig. 124) that the two processes may coexist. 

Type I.—Thus, there may be a history of intermittent claudication for 
many years (S. P., 65 years of age) with coldness of the extremities, even with 
attacks of thrombosis of the veins of one or both legs, with the development 
of ulcers and pain in the toes and foot. On examination, all of the vessels 
of both extremities may be found apparently closed. There is marked 
chronic erythromelia, marked reactionary rubor, ischemia and cyanosis. 
Pathological examination of the vessels in such cases will show the lesions of 
arteriosclerosis with the superimposition of secondary thrombi that are not 
of the thrombo-angiitis type. (Arteriosclerosis plus attacks of thrombosis.) 



432 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Type II.-—Most of the cases who have had symptoms for long periods 
failed to seek our advice before the advent of gangrene or trophic disturbances, 
frequently consulting the orthopedist or medical man who may be inclined 
to overlook the true nature of the trouble, diagnosticating flat-foot. They 
have pain in the calf of the leg, ankle or foot, particularly on walking for a 
long time. On examination, one or both feet appear to be blanched, this 
blanching extending for a variable distance over the dorsum of the foot, 
or a little farther up, depending upon the extent of the involvement, or it 
may simply affect the toes. With this, there are erythromelia, particularly 



Fig. 146.—Calcification of posterior tibial artery in arteriosclerosis. 

in the pendent position with or without cyanosis, absence of the dorsalis 
pedis, posterior tibial, and popliteal pulsations. The reactionary rubor comes 
on in the form of red patches. Associated are other evidences of 
arteriosclerosis. 

Such cases are difficult to distinguish from thrombo-angiitis obliterans 
or from associated thrombo-angiitis and arteriosclerosis. 

Roentgen ray examination is of great aid, firstly in the detection of cal¬ 
cified arteriosclerotic arteries (Fig. 146), and secondly, in estimating the 
amount of bony destruction present. In the arteriosclerotic affections of 
the vessels of the lower extremities, notably when attended with diabetes, 
the extent of the necrosis of bone is apt to be minimized by the clinician 


A R TERIOSCLEROSIS—DIAGNOSIS 


433 


when a mere sinus or small area of superficial gangrene is present. For, 
the disintegration not infrequently is more rapid and far reaching in the 
soft tissues, tendons and bone, than in the visible parts. It is the insidious 
progress of an indolent type of infection coupled with the deep necrosis 
that gives pictures such as are exemplified by Fig. 147 at a time when the 



Fig. 147.—Insidious destruction of bone with necrosis and gangrene, associated with 

arteriosclerosis. 


patient is still up and about, and quite unaware of the gravity of the situation. 
In such cases the Roentgen ray examination will demonstrate firstly, calcified 
arteries; secondly, atrophy of the bones of the foot, without the dis¬ 
appearance or blurring of the distal phalanges so characteristic of Ray¬ 
naud’s disease, and thirdly, destruction of bone. Such bone disintegration 
is not limited in extent as in Raynaud’s disease, but may involve many 
phalanges, the metatarsal and even the tarsal bones. 

L. G., male, 50 years of age (diabetic and arteriosclerotic) had had a sore fourth toe on 
the left side for some three months prior to October 6, 1915, this toe becoming gangrenous 
and separating. A sinus had persisted, attended with constant severe localized pain. 

Physical examination shows a suppurating sinus, marked, erythromeha, marked ische¬ 
mia on elevation and absence of the dorsalis pedis and posterior tibial pulsations. 

X-ray examination October 7, 1915, shows the dorsalis pedis and hallucis distinctly 
arteriosclerotic. The head of the fourth metatarsal and part of the shaft, as also about 
28 


434 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


one-sixth of its length at its distal portion, are completely destroyed. A faint indication of 
bone about the metatarsal phalangeal joint is still present. The shaft of the first phalanx 
of the third toe is very much thinned out, also being atrophic and involved. The distal 
part of the third metatarsal is also atrophic and disappearing, as well as the metatarso¬ 
phalangeal joint. , , , , . 

In short, destruction by necrosis of the head of the fourth metatarsal, atrophy and 
necrosis of the metatarsophalangeal (third), and marked atrophy of the first phalanges of 
the second and third toes. . ...... 

Diagnosis .—Arteriosclerotic process with gangrene and trophic disorders with infection. 

Except for the rare cases developing at a relatively early age (forty to 
fifty-five), the advanced age of the patient is significant.. The history of 
intermittent claudication, the absence of arterial pulsation, evidences of 
defective local nutrition, the development of trophic disorders, the blanching 
of the foot on elevation with occasional rubor in the pendent position, 
the presence of distinct calcareous vessels in the Roentgen picture, and finally, 
the development of trophic disorders followed or attended by severe pain or 
gangrene, are the chief points to be relied upon for a diagnosis. 

Although the chief clinical features of the disease, thrombo-angiitis 
obliterans, will be discussed later, the following differential points may be 
noted here. First, the symptoms in thrombo-angiitis obliterans, as far as 
the development of gangrene is concerned, are apt to come on much more 
slowly, the prodromal symptoms or signs lasting for weeks, many months 
or even years. Second, blanching and erythromelia (rubor) are not so regu¬ 
larly present in arteriosclerotic and diabetic cases, and if present, are 
usually not so marked. Third, gangrene may in either instance cover a 
small area at the beginning and slowly advance, but in arteriosclerosis and 
diabetic cases its advance is apt to be more rapid. Moist gangrene is less 
apt to occur in thrombo-angiitis obliterans. Fourth, alteration in the 
outward appearance of the limb in arteriosclerosis may be almost imper¬ 
ceptible before trophic disorders and gangrene develop, whereas in thrombo¬ 
angiitis obliterans the distinct evidences of the disease make their appearance 
many months previously. Fifth, the absence of migrating phlebitis, phle- 
bitic nodosities, so typical of thrombo-angiitis obliterans is of differen¬ 
tial value. Sixth, the occurrence of gangrene of the upper extremities is 
extremely rare in arteriosclerosis, relatively common in thrombo-angiitis 
obliterans. Seventh, racial (Hebrews), and sex (male) predilection so 
typical of thrombo-angiitis obliterans, does not obtain to a like degree in the 
arteriosclerotic forms. 


CHAPTER LXXII 

ARTERIOSCLEROSIS—PROGNOSIS 

In arteriosclerotic gangrene the prognosis is usually grave. In general, 
the outlook is related to the age (the older the patient, the more dubious the 
chances) and the general systemic condition. When extensive thrombosis is 
absent, threatening gangrene may be controlled either spontaneously by 
rest, or, with the aid of the proper therapeutic measures. Or, the patient 
may get well with the mere loss of a phalanx or digit. Patients of very 
advanced age, with extremely poor circulation, must be regarded as gravely 
ill, for high amputation, above the knee or at the middle of the thigh, will 


ARTERIOSCLEROSIS— TREA TMENT 


435 


eventually become necessary. Even this procedure when it is well borne, may 
be followed by continued sloughing of the skin flaps, necrosis of the exposed 
tissues and finally a lethal outcome. 

The outlook is always bad in cases of arteriosclerotic gangrene of the dia¬ 
betic type. As a rule we are dealing with patients advanced in years. The 
arteriosclerotic process is intense. The vitality seems to be diminished, both 
by virtue of the condition of the vessels, as well as by the general systemic 
condition of the patient. In spite of the best conservative treatment, 
failure to heal even a small ulcer is common, and extensive, subacute, phleg¬ 
monous formation is to be expected in many of the cases. Even when a 
line of demarcation has developed, the spontaneous sequestration of the 
part and spontaneous healing is only to be regarded with a degree of hope in 
those cases where but a small part is involved, such as a toe or a part of a 
toe. When amputation above the knee has to be performed in diabetics, 
the danger of supervening coma is great. 

This type of gangrene may be regarded as one of the least hopeful, the 
mortality being higher than in any other type of gangrene due to arterial 
disease. 

Since the adoption of the insulin (iletin) method of treatment, the prog¬ 
nosis has become distinctly better, both in so far as the prevention of coma 
and a lethal outcome are concerned, as well as in enhancing the patient’s 
ability to combat complicating infection. Perhaps with advances in the 
methods of administration of this substance, the outlook will be so much 
improved, that the gravity of impending coma will be greatly minimized. 

Pessimism as to the likelihood of local healing after amputation of a toe 
or after the advent of infection, should not be carried so far as to reject all 
possibility of the success of conservative measures. Indeed, it will be pointed 
out in the chapter on Treatment that astounding results may be achieved 
even in the diabetic cases without sacrifice of the affected extremity. 


CHAPTER LXXIII 

ARTERIOSCLEROSIS—TREATMENT 

The simple arteriosclerotic and diabetic cases may be considered together, 
although the special exigencies of the diabetic cases will require particular 
attention. Treatment includes the systemic therapy of the diabetes and 
generalized arteriosclerosis, and prophylactic treatment against complications. 
Local management comprises methods of enhancing circulation in the affected 
extremity, the care of trophic disorders, secondary local infection and methods 
of amputation. 

Prophylactic Measures. —The patients with diabetes as well as those with 
uncomplicated athero- and arterioslcerosis should be given a list of rules 
that must be carefully observed, to minimize the chance of developing 
trophic disturbances and gangrene. 

First, walking for great distances should be avoided, particularly if there is 
a history of intermittent claudication, cold extremities, previous attacks of 
gangrene, or trophic disorder, together with the objective findings by the 
physician pointing to impaired circulation, such as ischemia, pulseless vessels, 


436 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


or erythromelia. Second, exposure to cold, with possible frost-bite is danger¬ 
ous; even moderate degrees of cold are poorly borne. Third, the wearing of 
tight shoes should be carefully shunned. Wherever possible, a sojourn in a 
warm climate will be found beneficial. Fourth, all manipulations, such as 
cutting corns, callouses, ingrown toe-nails, bunions, should be left to a phy¬ 
sician or surgeon, for, the very beginning of trouble is often traceable to the 
manipulations of a pedicure. Fifth, the smallest injury should be scrupu¬ 
lously cared for by a competent surgeon. Sixth, daily cleansing of the 
feet, with more than ordinary care, and the use of sterile dusting powder 
should be insisted upon. Seventh, tobacco and alcohol should be indulged in 
with great moderation, or not at all. Eighth, diabetes, if present, should be 
treated according to present day methods with a view to making the patient 
free of acetone and diacetic acid and reducing the sugar content of the blood. 

Methods of Improving the Circulation. —These include, first, the author’s 
postural treatment; second, the hot air treatment; third, the diathermic 
treatment; fourth, the heat of electric lamps; fifth, the thermophore. 

All these methods may be given a trial. They are described under the 
section on thrombo-angiitis obliterans. They are not applicable, however, 
in all cases and only experience can teach us what the best methods may be 
in any given case. 

The postural treatment (author’s) which consists in the induction of a 
reactionary hyperemia in the affected part by preliminary elevation of the leg, 
followed by depression of the limb in a dependent position—may be 
used with some benefit in almost all cases, except where gangrene has already 
become extensive, where a phlegmon has developed, or where such changes of 
position are too painful to the patient. When recent extensive thrombosis has 
taken place, it is also contra-indicated. 

The postural treatment, or exercises to induce rubor and an accelerated 
circulation must be varied in its method of application in each and every 
case. The period of elevation should be the minimum amount of time 
necessary to produce a frank blanching of the foot. This is usually about 
30 seconds to 3 minutes depending upon the degree and extent of the vascular 
obstruction. The next period of depression (or of the hanging leg) is to be 
prolonged about 1 or 2 minutes beyond the time necessary for the induction 
of distinct rubor. An abridgement of this is then warranted, when the patient 
complains of increased pain in this position, or if the pain becomes unbearable 
after a given duration of time. The third position of rest in the horizontal 
may be extended at will beyond 3 minutes provided that this does not suffice 
to give enough repose to the patient. In general it should be longer in the 
atherosclerotic cases than in the younger people affected with thrombo-angiitis, 
since the former may find the treatment onerous unless sufficient intervals of 
rest are provided. 

The position of the resting limb in all forms of obstructive arterial disease is 
a matter that has, as far as the author knows, received no attention on the part 
of the clinician. If careful observations on the appearance of such limbs in 
varying postures be made, especially after the induction and abatement of 
reactive circulatory manifestations, it will be noted that the color of the foot 
varies considerably when in the horizontal plane. Whilst a normal or 
slightly diminished flesh color is not infrequently seen even in advanced 
arterial disease, the affected foot will often evidence varying degrees of 
pallor. This may affect but one or more toes, or the forepart of the foot, or it 
may involve even some of the distal portions of the leg. Or, the dorsum or 
plantar aspect of the foot may show patches of blanching alternating with 


ARTERIOSCLEROSIS—TREA TMENT 


347 


pinkish or slightly cyanotic areas. All of these color manifestations must be 
interpreted as attesting a circulatory insufficiency in this position. And as 
such, we may deduce lessons of prophylactic and therapeutic value—to wit, 
that such limbs are not to be allowed to stay during their period of rest, in the 
horizontal position, but somewhat depressed;, and just enough to bring about 
color evidences of circulatory activity. And so after testing the angle 
necessary to bring about the return of almost normal color, the patient must 
be instructed that this particular position is to serve as his horizontal. Indeed, 
it is well even when asleep to arrange the bed so as to conserve the angle 
previously arrived at. For, harmful as is the continued stasis induced by 
prolonged standing or walking, so also is one of continued ischemia, even if but 
slight. A position of elevation universally regarded as harmless must be 
avoided because of its depleting effect. 

The Duration of the Postural Treatment .—If the series of elevation, depres¬ 
sion and rest constitute a cycle, a repetition of these in the indicated succes¬ 
sion would comprise a seance. The determination of duration and number 
of seances daily must necessarily depend on the condition of the given case, 
and on the experience of the physician. In the atherosclerotic cases, we 
must restrict the length and number of seances somewhat. A good rule to 
follow is to alternate seances of about i hour with the application of some 
form of heat for one-half to three-quarters of an hour, allowing hourly 
periods of rest for meals and continuing the treatment well into the evening. 
If this be too onerous, time may be given for an afternoon nap of i or 2 
hours. The most reliable immediate measure of the efficacy of the method 
is the change in color in the leg, the appearance of trophic disorders, and the 
subjective state of the patient. All these should govern the treatment 
qualitatively. 

Hot air treatment must be very carefully applied, and should exclude 
the part affected by trophic disturbances or gangrene. The temperature 
should be gradually elevated, being no higher than 125 to 150 F. at the 
beginning of treatment, and raised no higher than 220°. Seances of 15 to 
45 minutes, 3 to 6 times a day have given good results. Great care must be 
exercised in the use of hot air to avoid burning the patient, since dire results 
may follow such additional insult to the already damaged part. Here too, 
in the presence of extensive gangrene, phlegmon formation, attacks of acute 
or recent thrombosis with threatened dry gangrene of a large portion of a 
limb, this method is contra-indicated. 

The application of heat by means of special lamps will find use where a 
hot air apparatus is not obtainable. So also an electric thermophore is a 
valuable aid to other methods of treatment, and should be wrapped around 
the thigh and leg over a flannel bandage, the temperature being controlled 
by a thermometer. 

The greatest care must be exercised in the use of hot air in the so-called 
baking apparatus or oven, both to avoid aggravation of the condition, and 
especially to escape the danger of producing burns. Any appliance of this 
sort should be set up and watched by a competent and conscientious nurse 
or attendant, lest the exposed and badly nourished skin come into contact 
with hot metal or with a lamp, with consequent jeopardy to the integrity 
of both skin and limb. 

Since we have employed the postural treatment, it has been found advis¬ 
able to alternate the seances with periods of hot air application, so that the 
number of each will vary. Where the exercises are well borne for an hour 
at a time, they may be followed by similar or slightly shorter periods of hot 


438 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


air. We no longer believe that the reactionary circulation induced by heat 
is sufficiently intensive or lasting to be of appreciable service when one or 
two short applications are given daily. Our aim should be to enhance the 
circulation over greater parts of the day and evening, an issue obtainable only 
through intensive, repeated and prolonged methods. And so, our present 
rule is to give at least 4 or 5 hot air treatments or approximately as many as 
the postural exercises and the bathing periods (in the cases of trophic ulcer 
and limited gangrene) as the case will allow. 

The diathermic treatment may be tried in the arteriosclerotic and dia¬ 
betic cases, if thrombophlebitis, extensive gangrene, phlegmon, ulcer, and 
infection are not present. It is, therefore, limited in its usefulness to those 
early cases in which symptoms of intermittent claudication are present 
together with threatened trophic disorders and gangrene, without actual 
gangrene or ulceration. 

Treatment of Trophic Disorders and Gangrene. —This includes (1) all 
those conservative measures which have for their purpose the attempts to 
heal trophic disorders, such as ulcer, infections and gangrene of small extent; 
and (2) methods of amputation. 

Wherever possible, particularly in cases of arteriosclerotic gangrene, 
complicated with diabetes, every effort should be made to prevent extension 
of the local process, and to bring about a cure without amputation. Absolute 
rest and strict asepsis are essential. Where dry gangrene is present, dili¬ 
gent attention to cleanliness of the part, sponging with weak alcohol, powder¬ 
ing with dermatol or bismuth subnitrate, are measures that are indicated 
until sequestration or demarcation begins. Where sloughs are present, no 
attempts should be made to separate these artificially unless this can be done 
without causing too much injury. Where infection is present, daily baths of 
warm saline solution from 15 to 20 minutes, 2 to 6 times daily, followed by 
sponging with weak alcohol over the intact skin, and then the application 
of wet dressings (liquor Burrowi 1 part, glycerin 2 parts, water 3 parts, or 
2 per cent boric acid) changed often, and kept moist without the use of 
impervious rubber tissue or other means, will tend to accelerate the separation 
of sloughs and limit the inflammatory process. Incisions must be made 
whenever there is an extension of the phlegmonous process, nitrous oxide gas, 
or nitrous oxide with oxygen being administered for this purpose. Local 
anesthesia should not be used under any circumstances. When a toe or a 
small part has become sufficiently loosened, the part may be removed under 
nitrous oxide gas. Or, when the gangrene is limited to one toe, or more, and 
the pain becomes too great to bear, the removal of one or more toes under 
nitrous oxide gas is indicated. 

Treatment According to Case Types. —Although no rigid rules can be laid 
down for the indication and manner of application of the various methods, 
each and every case warranting special modifications, a general survey 
may be given that will clarify the principles to be followed. Here as well as 
with all forms of therapy, the treatment depends on the clinical form, stage 
and intensity of the lesions. 

Let us divide the cases into 

(1) Those with intermittent claudication, or occasional pain, or coldness, 
without trophic disorders or gangrene. 

(2) Cases with evidences of arterial closure, that develop a minimal 
infectious lesion or trophic ulcer. 

(3) Cases with chronic ulcerative or perforative (perforating ulcer), 
lesions without progressive and profound infection (phlegmon). 


ARTERIOSCLEROSIS—TRE A TMENT 


439 


(4) Cases with any of the above and superadded attacks of thrombosis. 

(5) Cases with atrophy or chronic withering of the extremity with or 
without intense chronic rubor. 

(6) Cases with frank gangrene. ... 

(7) Cases with any of the above complicated by (a) indolent, or {b) 
severe infection (with lymphangitis and possibly general symptoms). 

(8) Cases with associated vasoneurotic crises may warrant trial of the 
Leriche operation (Chap. CV); these are described on pp. 578 et seq. 

1. Patients who come to us with the story of difficulty on walking, vague 
pains or coldness of the feet, will rarely submit to a rigid regime even though 
apparently insignificant symptoms may be of grave import. As soon as the 
diagnosis of chronic impairment and deficiency of the circulation is made, the 
general advice both as to the prophylaxis and active therapy should conform 
in its rigidness with the gravity of the situation. And not only should we 
take the extent of arterial occlusion—as evidenced by the absence of pulses 
—into consideration, [but importance should also be attached to the sigm- 
ficance of ischemia, rubor, and the angle of circulatory sufficiency. 

Where there is but very little pallor on elevation, little or no chrome 
rubor and the complaint of intermittent claudication is not marked, the 
importance of prophylaxis both general and local should be emphasized, and 
the evils that may ensue upon injudicious mode of living and excessive 
exercise should be brought to the patient’s notice. The postural treatment 
should be begun so as to occupy at least 3 hours of the day and at least 1 
(or 2) treatments with some form of thermic apparatus is to be suggested. 
The internal administration of iodides intravenously is lauded by some; 
and if there is any possibility of a luetic infection, antisyphilitic treatment 
is in order. For the well to do, a sojourn in a southern, warm climate during 
the winter months—during which time golf, sports, walking, tennis, etc. are 
to be interdicted—constitutes important prophylaxis. Massage is inadvis¬ 
able, since the advent or onset of thromboses can never be foretold. Periods 
of rest after meals, with removal of all foot covering other than loosely 
fitting slippers and socks, avoidance of personal cutting of nails and corns, 
scratching, etc., are points not too negligible to be forgotten. 

The question of “ How long may I stand on my feet? or How far may 
I walk?” is aptly put by the patient and deserves careful consideration and 
deliberation on the part of the physician, whose answer should be founded on 
a careful clinical study of each case. Where we suspect possibly thrombosis 
of deeper arteries, or where the pain is sudden and intensive so as to awaken 
the suspicion thereof, the patient should be put to bed at once for periods of 
1 to i weeks or more. Even thrombosis or thrombophlebitis of superficial 
veins—external or internal saphenous—may necessitate similar measures, 
and in such cases the manifestations due to disease m the superficial and 
deep vascular channels should be carefully balanced and appraised. < 

Here, too, as in all cases, the circulatory sufficiency in the horizontal 
position is to be estimated, so that correct advice as to posture when sleeping 
can be given. Whenever ischemia is present in the horizontal or very slightly 
elevated position, indicating that the encroachment ol the disease ' 1S thready 
of considerable extent, a moderate degree of downward obliquity of the limb 

(as previously ascertained) may be preferable. - . Tvnbhir 

2. Cases with Arterial Closure that Develop Minimal Infections or Trophic 
Lesions —With the principles laid down in the preceding discussion well in 
mind as applicable ina general way to all cases, variations depend on the com¬ 
plicating manifestations, degree of vascular inadequacy and infection. 


440 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Whenever a small, apparently insignificant cutaneous lesion appears 
in cases of disturbed circulation of the extremities (particularly if of organic 
vascular nature) its importance must not be minimized and corresponding 
prophylactic and therapeutic measures instituted. 

Fissures and abrasions are the least harmful, but also require special 
attention. Strict surgical asepsis and antisepsis are in order. Where an 
abrasion is clean, a dusting powder of dermatol or aristol is to be applied, but 
immediately to be substituted by wet treatment should evidences of infection, 
reddening, exudation and pain ensue. Fissures when in callous regions will 
heal most rapidly, if, after the edges have been softened by salicylic or soap 
salicylic applications (wet or plaster) these be pared down with a razor 
blade, so as to transform the deep cleft into a shallow wound. If the fissure 
be situated in an accessible region on the heel, margin of the foot (plantar 
aspect) and is absolutely free of infection, the plaster mentioned may 
be applied without hesitancy provided that it be removed and changed 2 or 
3 times daily and the wound inspected for the possible development of 
signs of inflammation. 

If there be a slight infection about or under a toe nail, the latter must be 
immediately cut in such a manner as to give free escape to secretions. Dress¬ 
ings (even wet) should not remain in contact for more than 1 or 2 hours at 
a time, and frequently saline foot baths (every other hour for one-half hour) 
will not only shorten the period of infection but encourage healing. Indeed, 
dressings of any kind over open wounds in these cases are dangerous unless 
they be very frequently changed, at least every other hour. Too much 
emphasis cannot be laid upon this statement; for many a limb has been 
sacrificed to the traditional apathetic and disinterested attitude of the practitioner 
in the local treatment of these cases. 

Besides the measures directed to foster healing of such surgical lesions, 
the usual general treatment is applicable. The postural and hot air methods 
also have their place; the extent of their administration being a matter of 
judgment in each and every case. 

3. Cases with Chronic Ulcerative or Perforative (.Perforating Ulcer) Lesions 
Without Progressive and Deep Infection (Phlegmons) .—Another, very valuable 
measure is at our disposal here, in the use of constant baths. Hot saline 
baths at temperatures from 95 0 to 105° F. are exceedingly valuable in these 
cases. Normal hyper- or hypotonic solutions of salt have been variously 
recommended. Indeed some would vary the concentration with the physico¬ 
chemical constitution of the blood serum of the particular patient treated. 
In general, slightly hypertonic solutions are advised. The baths are to be 
given either almost constantly during the day, or intermittently. Where 
infection has been kept in check, it is usually wise to alternate baths of 1 
hour’s duration with exercises and hot air treatment of similar length. The 
postural treatment is to follow the bath, and the bath to follow the dry 
thermal measures, in order to give the leg a chance to dry out before the 
heat is applied. Here, too, no inflexible rules can be laid down, for even the 
baths at body temperature, or the hanging position may be intolerable in 
certain instances. Should such be the case, an irrigation apparatus that 
flushes the parts with the foot at horizontal or almost horizontal is an apt 
variation of technic. 

4. Cases with Super added Attacks of Thrombosis. —We mean here particu¬ 
larly the sudden occlusive process in the deep arterial paths that may 
suddenly incapacitate the individual, or occasionally may be of slight sympto¬ 
matic severity and only recognizable through the rapid alteration in the 


ARTERIOSCLEROSIS—TRE A TMENT 


441 


objective state. In both, prophylactic treatment is to be carried out at 
once. The patient is to be put to bed, the affected part wrapped up in lamb’s 
wool or other warm protective covering, guarded by special devices against 
pressure sores either at the heel, calf or toes. A wire cage or guard over 
the leg, covered by a blanket, enclosing an electric lamp or electric pad, 
will keep the part at whatever elevated temperature we may desire. Atten¬ 
tion is to be directed to first, the state of the circulation during subsequent 
periods of each day and from day to day; second, the condition of the skin 
as to the effects of impoverished circulation for hemorrhages and lesions of 
impending necrosis; and third, for the arrival of that moment when active 
therapeutic measures for enhancing the circulation are to be initiated. 

The severest effects of arrest of circulation are usually in evidence shortly 
after the onset of thrombosis with such manifestations as pallor, coldness, 
blueness, pain and insensitiveness of distal parts. There are cases, however, 
in which aggravation of circulatory supply occurs gradually pari passu 
with an advancing thrombosis, or through failure of collateral supply, or 
as a sign that irremediable damage has been done. Leaving the discussion 
of the latter two eventualities for subsequent paragraphs, we are concerned 
here with the cases that improve spontaneously and with our aid. As 
warmth of the part and color return, we begin to estimate the degree of 
ischemia, the angle of circulatory sufficiency and the extent of closure of 
the palpable vessels (pulses in the two pedal arteries, popliteal and femoral). 
The rapid advent, too, of rubor is a valuable and indeed prognostic sign of 
good omen. As soon as pain has abated, we can employ a greater amount of 
heat, although excessive heat is always to be avoided. Then we may begin, 
gradually with the postural treatment but in modified and restricted fashion, 
limiting the periods of elevation to a minimum, as well as the time of depress¬ 
ing and we may extend considerably the period of rest. Again, it should be 
remembered that very soon after the onset, the horizontal position may 
have to be avoided if pallor is evident at this level. On the other hand, 
stasis also is objectionable, so that services of an excellent nurse will be of 
unusual worth during this critical stage. Whenever it appears that the 
veins stand out too prominently with the leg at a slightly oblique decline, 
it should be lifted up for a moment to give the outflow its needed opportunity. 
Baths are to be scrupulously avoided, and the skin may have to be rubbed 
with coca butter or vaseline, since even water and soap may not be tolerated. 
The integument may become thin, atrophic and dry, and the oil applica¬ 
tions are best borne. Minute hemorrhages and even small cutaneous 
necroses will often heal under dry treatment with non-irritating sterile dust¬ 
ing powders. 

As improvement occurs, the postural method may be more vigorously 
applied. Care should be taken to keep the patient off his feet for weeks or 
even months. Sometimes this type is only a transition into the condition of 
chronic “phthisis of the leg” or “atrophic painful red leg,” which may not 
tolerate ambulation for months, or which may permanently interfere with 
locomotion. 

5. Cases with Chronic Atrophy. —Very little can be done in a therapeutic 
way for this type of case. Some develop gangrene, others remaining in 
statu quo for months or years. If locomotion be almost altogether inter¬ 
dicted, many limbs will be saved for the longest possible period and indeed 
life may thereby be prolonged. 

6 and 7. Cases with Gangrene with or without Infection. —The various 
problems that confront us under these conditions have already been touched 


442 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

upon, and it remains merely for us to apply the principles laid down to con¬ 
crete clinical pictures. . 

Cases with Gangrene without Infection .—It need hardly be emphasized that 
no absolute restriction into such a category can be definitely prognosticated 
in any given case, since infection may ensue at any moment. Still within 
that period when there is gangrene of the dry or moist variety, the thera¬ 
peutic procedures applicable are sufficiently uniform to permit of concise 

presentation. # . 

In gangrene of the atherosclerotic variety, the treatment diners m 
essentials only as to whether complicating diabetis exists or not. 

Gangrene without Hyperglycemia. —The patient is confined to bed and is 
given the general tonic and systemic treatments, that the cardiac and metabolic 
status warrant. The application of the kind and intensity of local treatment 
will have to conform to the site and extent of the gangrene. With dry gan¬ 
grene of one or more toes, with a tendency to demarcation, an expectant attitude 
is best. The postural and hot air methods and the prophylactic measures 
previously alluded to, while the patient is in bed, on a couch or in a reclining 
chair, are excellent adjuvants in fostering limitation and demarcation of the 
process. Where, however, the gangrene is progressive and creeps over the 
dorsum of the foot, implicates several toes, and with the big toe involved 
ascends beyond the metatarso-phalangeal joint, the conservative methods 
will usually have to yield to radical surgery with ablation above the knee. 

When signs of infection appear—tenderness in a direction proximal to the 
gangrenous digit be it dorsal or plantar, followed by reddish, bluish or 
purplish discoloration of the overlying skin—or if a drop of pus appears 
in the immediate vicinity of any trophic ulcer, the dry gangrene becomes 
for practical purposes of therapy, equivalent to the moist type, and the 
continuous (or frequent) administration of baths is in order. The concealed 
foci must immediately be opened by adequate incision under nitrous oxide 
gas. Or, anesthesia may be wholly dispensed with when cutaneous sensi¬ 
bility has been destroyed by the subcutaneous and subfascial disintegrating 
and putrefactive process. Undermined skin can often be incised without 
causing pain. 

As the process becomes an infectious one, both postural and hot air 
treatments should be dispensed with; firstly, because they are difficult to 
carry out; and secondly, because they are attended with the danger of foster¬ 
ing extension rather than limitation of the infectious process. 

When the latter reaches a certain degree of severity and extent, when 
lymphangitis is superadded, and when the limb is already seriously compro¬ 
mised, or, when the general systemic symptoms and signs of intoxication 
begin to appear, we should not tarry any longer, and forthwith advise 
amputation. 

Gangrene with Hyperglycemia. —The problem becomes a more grave one 
here, and the state of the kidneys, heart, blood and urine must be carefully 
watched. The general medical treatment need not be dwelt upon other 
than to accentuate its great importance in determining the outcome. Not 
only must we estimate the sugar content of the blood, the presence of glucose, 
acetone and diacetic acid in the urine, and the C 0 2 combining power of the 
serum or the alveolar air; but the blood chemistry as an index of the renal 
function must be given careful attention. For the prognosis is bad, when 
there is renal insufficiency, cardiac weakness and marked acidosis. 

Of the many suggestions that have been made on the pre-operative 
treatment, the following seem to be the best: Theadministration of large 


ARTERIOSCLEROSIS—TREA TMENT 


443 


amounts of fluid, one glass every hour; thorough purgation with enema ta; 
avoidance of fats that may increase acid production; and the administration 
of oatmeal, alcohol and levulose—substances that are said to favor the 
combustion of ketones. 

Insulin .—The remarkable discovery of the therapeutic value of insulin 
(McLeod, Banting) bids fair to greatly improve the prognosis. Insulin 
may be administered hypodermatically for one or two days before amputa¬ 
tion is contemplated and continued according to indications for a variable 
time thereafter. 

Insulin is believed to be of great value both before and after operation. Although 
glycosuria may not disappear with its use, it is usually diminished and with the lessening of 
the glycosuria there is a fall in ketone bodies. Infection increases the gravity of diabetes; 
insulin lessens the danger of surgical intervention (Joslin). 

To diminish the risks of acidosis and to limit the extension of this type of 
gangrene, we must intervene early to combat infection and especially the cold 
type of puriform gangrene that so insidiously creeps on through the deeper 
tissues. Tenderness, fluctuation, discoloration, bogginess and puffiness 
must be sought for early and along the line of such objective signs, incisions 
must be made at timely moments. Digits should be removed as soon as they 
are gangrenous and tend to obstruct the adequate outflow of pus or gangrenous 
products that are apt to accumulate in the plantar aspect of the foot. The 
permanent or intermittent bath too, with or without use of the Carrel- 
Dakin solution is indicated. 

The most valuable contribution to methods of treating this type of case 
was the discovery of insulin (iletin) which has justly found wide applica¬ 
tion in both the medical and surgical diabetic patients. 

Surgical Treatment. —The more conservative methods have already 
been discussed, so that we may confine ourselves here to the utility of 
amputation. 

Amputation .—Indication for amputation will depend upon whether 
conservative measures are successful or not, upon the general condition of 
the patient, and on the severity of the pain. It will, furthermore, be influenced 
by the rapidity with which the gangrene extends, and by the presence of a 
very extensive phlegmon that does not become arrested by conservative 
incision. 

There seems to be no unanimity of opinion regarding just where and when 
to amputate in cases of this sort. In general we may say that when conserva¬ 
tive treatment has failed—which includes methods of enhancing circulation, 
conservative incisions, dressings, and amputation of small extent when 
gangrene shows evidence of progression, when no line of demarcation forms, 
and the suppurative process threatens the patient, then amputation above 
the knee, preferably at the lower third or middle is to be performed. This 
should be done under nitrous oxide anesthesia, by the circular method, the 
aperiosteal type of amputation being preferred. The femur should be cut 
high enough so as to avoid the production of a conical stump, when the flap 
retracts. Since we may expect slight sloughing of the periphery of the flap 
even in favorable cases, it is wise to make provision for this in advance. 
The wound should be left fairly wide open, although several catgut sutures 
may be placed into the muscles to bring them together and control bleeding. 
Sterile adhesive plaster may be employed to approximate the edges of the 
flap loosely, wide drainage until granulations have formed, giving the best 
results. 


444 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

The results of amputation through the thigh are fairly good—as to mor- 
tality—in the non-diabetic cases, but the issue becomes progressively more 
grave in direct proportion to the age of the patient. In arteriosclerotic 
gangrene (even without hyperglycemia) any ablation below the knee is 
so dubious in its outcome as far as ultimate healing is concerned, that we 
recommend nothing but the high amputations through the femur. Such an 
intervention in the aged, needless to say, is sufficiently grave to awaken strong 
doubts in the minds of the immediate family as to the outcome; all the 
more so, since the high mortality of amputation in the neglected diabetic 
cases is a matter of common knowledge even amongst the laity. It is 
this attitude of the people and even of the average internist that is largely 
responsible for much neglect and procrastination, and indeed plays no sub¬ 
sidiary role in determining the eventual issue in a large percentage of the 
cases. 

What shall be our attitude regarding the advisability of high amputation 
in a given case; and when shall we be warranted in deciding that local 
operative and restricted ablation of smaller parts (toes) will no longer suffice ? 
The cases must be divided into the non-diabetic, young and old; and the 
diabetic, young and old, severe and mild. 

The Pure Atherosclerotic (•without hyperglycemia) .—In the patients from 40 
to 60 years (approximately) with good heart action, with renal adequacy and 
not too accentuated generalized atherosclerosis, we have been so well satis¬ 
fied with the relatively low mortality of high amputation, that our fear of 
this operation will not deter us from recommending it at an early date. 
And so we are justified in resorting to it, when amputation of the big toe for 
gangrene, perforating ulcer or chronic trophic disorders does not avail, and a 
chronic suppurating sloughing wound with or without progressive gangrene 
but with much suffering—results; also when a similar condition follows ulcers 
and gangrene of several of the smaller toes; or when with any local nutri¬ 
tional disorder, rapid, ascending infection, with or without lymphangitis and 
general toxicity occurs; or when there is massive dry gangrene of toes and a 
part of the foot; or when embolic or thrombotic processes lead to extensive 
dry gangrene of the foot and leg. 

In the older individuals because of the high mortality, and the dubious 
local outcome of the wound through the thigh, our inability to promise 
much to the family and the prejudices previously alluded to, account for the 
even greater percentage of failures than we would otherwise expect, were high 
amputation conceded as best and permitted much earlier after the onset of 
the gangrene. Here, just as with the cases of “ diabetic” gangrene (so-called) 
the author holds the view, that when once our clinical judgment tells 
us that the part can no longer be saved, amputation had best be done early, 
rather than late. For, the ensuing sleepless nights, the toxic absorption and 
continued suppuration are the factors that increase the mortality. 

The Cases with Hyperglycemia. —In general we may say that here the 
intensity or gravity of the diabetes and the renal condition play a greater 
role in the outcome than the age of the patient. Attention has so often been 
directed to the excellent results following conservative treatment with 
limited amputation of phalanges or whole digits and multiple incisions for 
phlegmonous processes, that the physicians as well as the surgeons’ judgment 
and activities have become hampered, their ardor cooled, and their usual 
boldness converted into an attitude of apathy or even repugnance towards 
any radical measures. We cannot lay down rules by means of which the 
surgeon can conclude when the conservative incisions and other measures 


MISCELLANEOUS AFFECTIONS OF THE ARTERIES 


445 


will have failed. For, this is a matter of experience and clinical judgment. 
Exceedingly important as a prophylactic measure is the admonition, that the 
incisions above an area of gangrene or only threatening gangrene should not 
be delayed and all accumulations of purulent and gangrenous material pre¬ 
vented. When, however, with the most spirited form of local treatment 
the process is not arrested, or when by reason of massive gangrene naught is 
to be expected from such restricted measures, we believe that high amputa¬ 
tion should be advised as early as possible. 

We believe that the mortality could be considerably reduced by the 
exclusion of that immeasurable, indeterminate but still vital complex of 
deleterious factors that are engendered and accumulated by the ever growing 
infectious and gangrenous foci. Abolition of these toxic elements cannot be 
brought about by baths and incisions in many cases; although a diminution 
of their potency, it is true, is thereby attainable. Whilst conservatism may be 
appropriate in some cases, there are many in which despite such means, the 
above mentioned elements constitute a growing menace, cumulative in action, 
and determinative in upsetting a balance, which early operation might have 
been able to conserve. 

With the prognostic sense of the surgeon well developed, and aptly and 
timely exercised into an expression of courageous conviction, and with the 
prejudices of the family overcome, many more lives could be saved by early 
intervention. 


CHAPTER LXXIV 

MISCELLANEOUS AFFECTIONS OF THE ARTERIES 

For the sake of completeness, brief reference must be made to certain 
other less common vascular lesions with which necrosis or gangrene may be 
complications. These are (i) simple hypertrophy of the vessels that does not 
per se either cause internal or external necrosis or gangrene; (2) tuberculous 
lesions that produce such effects internally; and (3) aneurysms which may, 
especially through complicating thrombosis give some or many of the symp¬ 
toms of the other obstructive vascular affections. 

The following are the results of some of the more recent pathological 

investigations on arterial lesions. . 

Pathology— In a general way the non-traumatic lesions of bloodvessels 
are referable 1 to (1) disturbances of nutrition; (2) disturbances of growth and 
development; (3) toxic effects; (4) infection (bacterial in general); and (5) 

special infectious agents. ,, , . . 

1. Lesions of Disturbed Nutrition .—When the blood supply is partly or 

completely in abeyance, alterations in the vessel wall may take place, buch 
changes are usually of embolic or thrombotic nature. The elements of t e 
vessel wall may undergo necrosis, or (in anemia) may show the presence ot 
fat, hemorrhage and weakening of the walls. , 

2. Disturbances of Growth and Development.—Here belong atrophy 
regressive changes, and hypertrophy. The latter will receive more detailed 
discussion later, since this pathologic process may be of some importance 
amongst the changes that occur in the arterial affections of the extremities. 

1 In part of this grouping the divisions suggested by Mallory have been adopted. 


446 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Atrophy may result as a senile change with spontaneous disappearance of 
the mural elements including elastic fibers and muscle cells with substitution 
of connective tissue. Usually such change is more apt to follow occlusion due 
to thrombi when the wall of the vessel may become converted into connective 
tissue, and even become hyaline. Other regressive changes, including sclerosis 
calcification, fatty degeneration, concern us here, only in so far as they form a 
part of the process elsewhere described as athero- and arteriosclerosis. 

3. Toxic Lesions .—These may attend the infectious processes, and have a 
special affinity for the arterial system. Diphtheria, scarlet fever, pneumonia, 
streptococcus infection—all are believed to produce toxins that may injure 


Fig. 148. —Artery—heart. Acute infectious lesion; necrosis, fibrin formation, leukocytic 
infiltration; yielding of wall forming infectious aneurysm. (Mallory.) 



the vessel wall, cause fatty degeneration of the cells, hyalin change or 
necrosis. Often there is a tendency to focal distribution, which cannot be 
explained, and, according to Mallory, is not dependent upon the vasa vasorum. 

4. Infectious Lesiqns .—These depend upon the immediate presence of 
pathogenic organisms. The histologic alterations vary with the type of 
infecting organism. There may be acute lesions due to the pyogenic organ¬ 
isms, with destruction of vessel wall and abscess formation; or, when the 
organisms are less virulent and die off readily, less intensive lesions are 
produced. 

Infection of the blood vessels may take place from without by continuity 
or through the adventitia and vasa vasorum , or from within. The inflam¬ 
matory reaction on the part of the blood vessels is said to be due either to the 
organism itself, the toxin derived therefrom, or to the injured cells. 

Leukocytes may accumulate under the endothelium of the blood vessel 
in acute infectious processes and especially as the result of the action of the 




HYPERTROPHY OF THE ARTERIES 


447 


glanders bacillus. Endothelial leukocytes and lymphocytes may accompany 
them. 

Mallory believes that the resulting formation of fibrin when undissolved 
by ferment and not eliminated, may cause proliferation of fibroblasts. In 
this way thickenings are produced that may be of injurious nature. An 
excellent example of infectious lesions in an artery from the heart of a case of 
streptococcus infection is seen in Fig. 148. Here a focal infection of the wall 
with necrosis, fibrin formation and leukocytic infiltration is depicted; the wall 
at this point shows the beginning of the development of an infectious type of 


aneurysm. 

5. Special Infectious Agents .—Here may be mentioned the results of blood 
vessel infection due to certain organisms that bring about lesions of special 
types. These are the glanders, leprosy bacillus, the treponema pallidum and 
the tubercle bacillus. The lesions of the last two are discussed in special 
sections. The pathological process of periarteritis nodosa, probably of infec¬ 
tious origin is also separately described. 


CHAPTER LXXV 

HYPERTROPHY OF THE ARTERIES 

Although this affection does not lead to gangrene, we should be aware of 
its existence, since it may accompany diseases that are thus complicated. 
One of the forms of hypertrophy affecting arteries that has been confused with 
obliterating endarteritis, gives pictures that have ofttimes been mistaken 
for the end products of organization of thrombi. For purposes of differen¬ 
tiation, therefore, it is well to know something regarding these hypertrophies 

or obliterative changes springing from the intima. 

Hypertrophy of the arteries may be a functional response, and difficult 
to differentiate from pathological conditions. The process may affect vessels 
active in collateral circulation, as well as the new formed and old. vessels m 
neoplasms. In chronic hypertension hypertrophies of isolated portions of the 
vessel wall may take place. Proliferation of the muscularis and new forma¬ 
tion of the elastic fibers are described. . 

Hypertrophy of the connective tissue within the vessel wall is of patho¬ 
logical significance. A slight degree of proliferation of the connective tissue 
in the intima is considered to be physiological. The endothelium (which m 
the foetal vessels lies directly against the internal elastic coat) is gradually 
displaced by proliferation of cellular connective tissue as time goes on. At 
first this connective tissue shows no tendency to the formation of sclerotic 
lamella. This proliferation is considered as a regenerative process in 
substitution for interruptions in vascular continuity. They are seen where 
cicatrices follow traumatic lesions. As a compensatory process proliferation 
here may occur in many diseases of the vessel wall, and goes on so slowly and 
constantly, that it is not observable until the finished product is striking. 
Again, proliferation of the intima is also regarded as a disease per se in cases 

in which no cause can be found. , . 

The process seems to proceed in the following manner Although it 
was first believed that the cells appearing between the endothelium and elastic 


448 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


coat are derived from the endothelium, it is now generally accepted that the 
fibroblasts may have their origin in the deeper layers of the vessel wall, 
penetrating the fenestra of the elastica. At first stellate and spindle celled 
elements appear. Then the loose connective tissue becomes denser and 
lamellated. If degenerative processes are absent, then this tissue develops 
elastic fibers and its own elastic system. 

In this way a tissue is formed that serves as the chief element in resisting 
dilatation of the vessels. Such tissue increases the central resistance (resis- 
ance to distension) of the vessels, and is unable to accommodate itself to 
the varying size of the lumen, as the normal vessel tissue can. It therefore 
acts as a distinct obstructive element to the circulation. 

In short, a sclerotic process in the vessels is thus formed, that leads to 
partial obliteration, particularly in the smaller ones, where it is regarded as 
an obliterating endarteritis. It is not believed that this productive process 
is a disease per se, but the response to numerous different provocative 
processes. 


CHAPTER LXXVI 

ACUTE ARTERITIS 

Acute arteritis affects either the visceral arteries, the arterioles, or the 
larger arteries, such as the aorta and those of the extremities. When it 
follows infectious fevers it is not apt to be generalized, but tends to be limited 
to certain territories. 

The subject of arteritis has received relatively little attention. We are 
concerned here especially with those lesions that are believed to produce 
peripheral circulatory disturbances either immediately, during the acute stage 
of the process, or subsequently by reason of thrombosis or other secondary 
mural changes in the arteries. 

The investigations of Wiesel on the arteries during the course of infectious 
diseases—such as diphtheria and scarlet fever—have demonstrated that 
distinctly recognizable alterations in the vessels occur. In the course of these 
maladies the changes manifest themselves in the form of a degenerative 
process in the smooth muscle and the elastic fibers. Usually the process 
begins in the media and is for the most part confined to this coat. The 
degeneration is focal, may occur in numerous situations and lead even to 
veritable necroses of the vessel wall in the severe cases. Such necroses may 
heal with resulting cicatrices, or a return to the normal may take place. 
When the intima is involved, permanent alterations occur. Even macro- 
scopically recognizable lesions may develop. 

Any of the arteries of the vascular system may be affected from the largest 
to those of the caliber of the digital arteries. Two groups have been 
described: (i) processes with marked participation of the elastic elements 
(diphtheria, typhus and pneumonia, influenza); and (2) those in which the 
musculature is particularly implicated (as in scarlet fever and septic diseases). 

The changes here described are not those of beginning arteriosclerosis. 
Distinguishing features of arterial lesions in the acute infections are the 
primary localization in the media, and confinement to this layer in most 
instances. Nor do the arterial lesions of syphilis usually begin as an infecti- 


ACUTE ARTERITIS 


449 


ous arteritis. But in the experimental vascular lesions produced by adrena¬ 
lin injection into animals, the characteristic change is often a primary necrosis 
of the smooth muscle and the elastic elements of the media. Intima 
changes are secondary or late. In this respect the arterial affections of the 
acute infectious processes resemble that of the experimentally produced 
arteriosclerosis. 

Etiology.—Acute arteritis of the extremities usually complicates the 
period of convalescence after typhoid, influenza, cholera, and scarlet fever. 
In typhoid fever the inflammation of the arteries is said to appear about the 
end "of the third week, or even later, and may be attended with thromboses. 
Gangrene of the extremities may result by reason of the acompanying com¬ 
plicating obturating thrombosis, although in some of the reported cases 
embolism may have occurred. The lower extremities are those usually 
affected, more commonly unilaterally; and the femoral, popliteal, posterior 
tibial, more rarely the external iliac and anterior tibial or pedal arteries 
are affected; in the upper extremity, the brachial artery. 

Influenza is next in frequency as a cause of acute arteritis. Here the 
femoral and popliteal arteries are most often affected; then the brachial 
and axillary. Gangrene has been observed in about two-thirds of the cases. 
In typhus fever also, gangrene due to arterial changes and thrombosis is 
not uncommon, the femoral artery being usually diseased. 

In acute articular rheumatism, the aorta, carotid, axillary, and brachial 
arteries are described as being the seat of arteritis. Even aneurysms of the 
posterior tibial and radial may be developed. Some authors account for 
the lesions in this malady rather as due to an embolic process than to pri¬ 
mary affection of the arterial walls themselves. And so, the cases of gangrene 
described are, therefore, interpreted as resulting from thrombotic or embolic 
occlusion. Gangrene of the extremities complicating arteritis may occur 
with puerperal infection 1 and pneumonia. Similar observations have been 
made in scarlet fever, and thrombosis of the popliteal is reported in cases of 
smallpox. 

Even in erysipelas during the convalescent period thrombosis of the 
popliteal may be a complication; in cholera it is not infrequent to find gan¬ 
grene due to arterial thrombosis. Similar observations have been made in 
dysentery, appendicitis, peritonitis, angina and gastroenteritis. . In advanced 
tuberculosis thrombosis of the arteries has been reported involving the 
extremities with the brachial, subclavian and tibial arteries affected. 

Pathology.—There may be localized thickenings of the intima with 
limited or circumscribed prominences (Roger and Gouget). In these there 
is cellular proliferation beneath the endothelium with various types of cells; 
one being large connective tissue cells with processes, another, type, more 
numerous, consisting of round cells. In cases where the lesion is more 
intense, the middle coat may be affected, but usually to a lesser degree. The 
internal elastic lamina or membrane may be irregular and fragmented, and 
leukocvtes surround new formed capillaries. The latter have their source in 
vessels' that penetrate from the external coat, causing a certain amount of 
disintegration of the muscular and elastic fibers of the media. In some 
infectious diseases the lesions of the middle coat may predominate (diph¬ 
theria, typhoid, grippe, scarlet fever, rheumatism); and Wiesel describes 

necrotic foci. , 

The external coat is said to be either uninvolved, or the first to be affected. 
Inflammatory processes in the vasa vasorum with perivascular leukocytic 
1 Wormser, Wien. klin. Rundschau, 1904. 


29 


450 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


infiltration and proliferation of fixed cells have been noted. However, 
all three coats may be eventually implicated. 

In a general way the lesions are similar to those of acute aortitis, except 
that in the latter the intima may appear intact, and smooth, but covered 
with gelatinous plaques and without thrombosis. In the arteries of the 
extremities, however, the clotting process is more apt to occur by virtue of 
the smaller size of the vessels and the retardation of the blood stream. 

Usually a clot will adhere to the affected region, at times insufficient to 
obliterate the artery; but more frequently secondary clot formation (accre¬ 
tion, stasis or stagnation clot) leads to obliteration of the artery, with exten¬ 
sion of the thrombotic process towards the periphery (also centrally) and 
even into branches. By reason of the rapid extension of the clotting or the 
thrombotic process it is difficult or often impossible to distinguish the primary 
seat of the clot formation. Only at autopsy is this possible, when a more 
nearly correct appraisal of the age of the thrombus can be made macro- 
scopically and microscopically. Organization of the clot usually follows. 

As a result of thrombotic obliteration, gangrene has been observed in 
the extremities, and infarction in the internal organs. 

Symptomatology.—Although arteritis may involve the visceral arteries, 
we are concerned here merely with those of the extremities. The best 
opportunity for studying the symptoms of this malady is offered, in the 
course of infectious diseases. The following description given by Roger and 
Gouget is typical of the acute manifestations of arteritis of the peripheral 
vessels: 

Although the manifestations may begin without apparent cause, their 
inception is usually referred to an untoward or brusk movement. The 
patient experiences sudden pain in the affected limb along the course of one 
of the larger arteries. The pain may be localized, may radiate throughout 
the limb, is intensified by motion, and tenderness can be elicited along the 
course of the artery (usually in the axilla, in Scarpa’s triangle, Hunter’s 
canal or in the popliteal space). Increase of temperature usually occurs 
simultaneously with or immediately after the onset, and also, sensory and 
circulatory disturbances in the peripheral parts. 

At first, paresthesia, formication or intense pain in the toes and calf of 
the leg are experienced. The pulses below the point of obliteration may 
be absent or diminished, some of the arteries being converted into hard 
painful cords. The symptoms vary with the site of the obstruction and the 
artery involved. Then the usual symptoms common to arterial blockage 
may be evolved; and even gangrene. Usually, however, the collateral cir¬ 
culation is sufficient to prevent extensive mortification. An intermittent 
course was reported by Eichorst and Mornet, in a case of arteritis due to 
influenza. In this instance the affected limb was found cold and partially 
anesthetic, the pulses imperceptible on one day; and on the morrow improve¬ 
ment took place with increased warmth, restored sensibility and pulsation. 
Then again, there was a recurrence finally followed by gangrene. 

In some cases the course is a rapidly progressive one, as if an embolic 
lesion had occurred: suddenly the patient experiences a tearing pain, the 
affected member becomes pale and cold, and gangrene is the issue. 

In an interesting clinical observation which was regarded by Dr. E. Libman and Dr. I. 
Strauss as one of arteritis following scarlet fever, there was a history of sudden cramp in the 
legs, both becoming cold, white and ischemic, in a child 5 years of age, 9 days after the 
beginning of the disease. There appeared to be no circulation below the knees; there was 
pain in the right great toe; but the circulation was restored during^the following,24 hours. 


ACUTE ARTERITIS 


451 


About this time there was a right sided hemiplegia which was referred to a similar process 
in the cerebral arteries. 

Rheumatic Arteritis.—The literature affords sufficient data to warrant the 
view that inflammation of the arterial wall may occur with rheumatic infection. 
In the aorta the intima has been found to present yellowish plaques of a 
gelatinous nature, occupying a part or the whole circumference of the vessel 
wall of the aorta and large vessels. Such areas, when situated in vessels of 
smaller caliber, may produce considerable narrowing and predispose to 
secondary thrombosis. Later, degenerative changes and calcification may 
convert such plaques into areas indistinguishable from atherosclerotic patches. 1 

Microscopically the lesions of the intima comprise proliferative changes 
in which the connective tissue cells with some leukocytes play the most 
important role. The cells are sometimes described as of embryonic type. 
The endothelium covering the plaques is intact in most cases. 

Characteristic changes have been noted in the media. The muscle fibers 
suffer the most intensive alteration. These show degenerative changes, and 
may disappear altogether leaving only the elastic fibers and a few degenerate 
nuclei and polynuclear cells. These necroses have been attributed to the 
toxins of rheumatic infection. 

As for the adventitia, a periarteritis is described and is believed to play 
an important role in the sensory symptoms. 

Symptomatology. —In view of the common incidence of rheumatic fever, 
acute lesions of the arteries are rather rare. The following arteries may be 
mentioned in order of decreasing frequency of involvement: the aorta, the 
carotid, the brachial and subclavian, the axillary, and the coronary. Least 
frequent of all, is the involvement of the vessels of the lower extremities. 
In this regard this affection is distinguished from the arteritis complicating 
typhoid and other infections in which the arteries of the lower extremities 
give most frequent evidence of disease. 

The first manifestation that attracts the notice of the clinician is the pam, 
which is constantly mentioned in all reported cases. It is spontaneous, 
localized in the region of the affected vessel and the least contact with the 
latter may augment and markedly intensify the suffering; sometimes acute 
exacerbations of paroxysmal nature may occur. 

A moderate degree of fever and increased rapidity of pulse may 
accompany. The French authors speak also of an exaggerated pulse in the 
arteries, and attribute it to a dilatation of the vessel through muscular relaxa¬ 
tion. Later, however, this gives way to diminished pulsation, due, in the 
case of the smaller arteries, to narrowing of the lumen. Sometimes, however, 
dilatation of the arteries is observed. Even an arterial murmur has been 
described as audible over the vessel. These are the symptoms referable to 
arteritis without obliteration, a type of arteritis described as parietal arteritis 

In the obliterated arteries , the radial pulse may completely disappear, and 
the arteries become transformed into hard fibrous cords. There may be 
associated coldness of the peripheral parts (usually the hands). Later, the 
affected member becomes pale, flaccid, diminishes in size, the hand becomes 
atrophied, and the nails show dystrophic changes. Sensory disturbances 
with diminished sensation to heat and pain are attendant symptoms. 

Clinical Course and Prognosis. —In the benign forms, spontaneous cure 
occurs, and after 2 weeks the pain disappears, the arteries returning to norma . 

1 Offering plausible basis for the infectious theory of the pathogenesis of 
atherosclerosis. 


452 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


At other times there is a tendency to multiple invasion of arteries, the patient 
finally succumbing with cerebral symptoms. 

When an obliterating arteritis develops, dry gangrene of the part may 
possibly be the issue. Definite cases of such gangrene are not reported, 
although imminent mortification and trophic disorders appear in the reports 
in the literature. Other eventualities are aneurysmal dilatation or a chronic 
arterial change that leads to arteriosclerosis. 

Rheumatic phlebitis 1 may appear after the articular manifestations. 
With sudden onset, sometimes preceded by chills, malaise, and elevation of 
temperature, it may have a migrating tendency, and affect numerous veins 
in different parts of the body. Just as in the case of the arteries, there may 
or may not be obliteration of the veins. A late edema of the peripheral 
parts is observed in some cases. Out of 27 cases observed by Schmidt, the 
lower extremities were involved 15 times the upper once; in one case the veins 
of all 4 extremities were implicated. These observations are in contrast to 
those of rheumatic arteritis where the upper extremities are most frequently 
affected. 

Acute Arteritis of Unknown Origin. —In an interesting recent communi¬ 
cation, Kramer 2 describes a case of gangrene in a child, due to arteritis with 
thrombosis and not preceded by a definite infectious disease. The clinical 
picture at the onset was that of purpura of either the hemorrhagic or fulmi¬ 
nating type. There was a sudden onset, injected throat, leukocytosis, then 
purpura, extensive ecchymosis and finally gangrene of one leg; the patient 
recovered after amputation, and the nature of the infectious process 
responsible for the arteritis could not be determined. 

E. H., white, male, 8 years old, was admitted December 7, 1920 (Dr. Solis Cohen’s 
service) with a provisional diagnosis of purpura. One week previously the boy complained 
of headache, became restless and feverish, and vomited twice. The patient was very pale. 
Two days later purple blotches appeared on the knees and outer aspects of both legs, and 
later, on the body as well. 

Physical examination revealed an injected pharynx, enlarged and injected tonsils. The 
extremities showed ecchymotic patches with sloughing. The left leg was the worse, the 
foot being blue, the toes cold and bluish black in color. No pulsation of the dorsalis pedis 
could be discerned. The temperature on admission was 99 0 F.; later it went up to 104°. 
The pulse range was from 90 to no. There was leukocytosis 26,400; polymorphonuclears, 
81 per cent. The blood culture was sterile. The throat culture showed streptococci. 
The patient’s condition became steadily worse. Gangrene developed in the left foot. 

Amputation was done above the knee on December 31, about three and one-half weeks 
after the patient’s admission. Convalescence was slow, but recovery finally ensued and 
(January, 1922) the lad was robust and enjoying good health. The limb was studied by 
the histologist, Dr. W. P. Belk, who reported as follows. 

Pathological examination. The large arteries showed a thickening of the media, 
which was due to a moderate proliferation of fairly young connective tissue cells. There 
was also a moderate amount of round cell infiltration in this arterial coat. At one point one 
large artery showed what appeared to be a very early and slightly marked necrosis. Oppo¬ 
site this there is a thrombus firmly attached to the intima. The endothelial coats at this 
point have been lost. 

In all sections the small arteries showed a more advanced pathological process. The 
thickening—still chiefly of the media—was great, resulting in the narrowing of the lumina to 
about one-third or more of the original diameter. 

It is quite conceivable and doubtless true that arteritis of unknown 
etiology, may be responsible for some of the phenomena of disturbed circu¬ 
lation occasionally encountered during adult life. For, gangrene is not 
always the immediate issue but occluded vessels may predispose later in 
life to circulatory deficiencies whenever the vascular paths become still 

1 See Chap. LXXXI, Miscellaneous Varieties of Migrating Phlebitis. 

2 Kramer, New York Med. Jour., Oct. 4, 1922, p. 394. 


ACUTE ARTERITIS 


453 


further compromised. Such added lesions may be bland thrombosis, 
thrombo-angiitis, arteriosclerosis and some of the other obstructive pro¬ 
cesses elsewhere described. 

In a study of other sections 1 the author found that in one of the larger 
arteries a large area of necrosis occupies a fair portion of the wall involving 
all of the coats. The muscle cells showed extensive degeneration. The 
presence of wandering cells suggested that an inflammatory reaction had 
been present, at least at the onset, in this zone. The immediately adjoining 
portions of the arterial wall show the most intensive proliferative reaction 

(Fig. 149)- 



Fig. 149.—Arteritis with mural necrosis; above, there is a zone of necrotic wall, bounded 
on the right by vascularized, inflamed media; below, occluding clot. (Kramer and 
Krumbhaar ) 

In this area bordering on the necrotic portion there is edema and slight 
degeneration, proliferation of all of the cells, and separation of the muscle 
fibers partly by the new formed capillaries. In other portions of the arterial 
wall, numerous new formed capillaries run in a more or less circular direc¬ 
tion thereby causing thickening of the arterial wall, the process diminishing 
as we trace it away from the necrotic zone. Inasmuch as these changes are 
intensively present where the occluding clot still shows no evidences of 
organization, it is fair to assume that they are the response to the primary 
changes in the arterial wall (the so-called arteritis). From the sections at 
hand it would seem that these primary alterations were a combination of 
focal necrosis and inflammation, and that the lesion seen in the section 
(taken from the leg 3 weeks after the onset of the disease) represents rather 
the attempt at healing than a specific inflammatory process per se. 

1 Received by author through the courtesy of Dr. Kramer and Dr. Krumbhaar. 





454 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Arteritis with Thrombosis Simulating Thrombo-angiitis Obliterans. 

Symptoms identical with thrombo-angiitis obliterans, but with a different 
clinical course, confined to one of the upper extremities, may present a clinical 
picture the classification of which may be difficult or impossible. Mani¬ 
festations including all the symptoms of impaired circulation, with occlusion 
of the brachial, radial, or ulnar arteries, trophic disturbances, ischemia or 
rubor, may follow insidiously after a history of acute infectious disease 
(influenza). Without reliable clinical observations the relationship between 
the previous infection and the occlusive condition of the arteries may not 
be clear. 

In short, symptoms identical with those of thrombo-angiitis obliterans, 
but of rather rapid development, confined to an upper extremity may be the 
evidences of occlusion of the large arteries, the result of either an acute 
arteritis with thrombosis, or acute thrombo-angiitis obliterans. The follow¬ 
ing case may be of interest. 

T. C., Italian female, 29 years of age, suffered an attack of influenza in January, 1922, 
after which variations in temperature of the right upper extremity were noted, most marked 
in the index and middle fingers. The color of this extremity was inconstant, varying from 
a dusky hue to red and white. One week after plunging the right hand into warm water 
(December, 1922) because of its constant cold feeling, an ulcer appeared at the tip of the 
middle finger. 

Physical examination, January 29, 1923, reveals general atrophy of the right hand and 
forearm. The tips of the fingers of the right hand are discolored, and an area of necrosis 
over the tip of the middle finger is in evidence. The fingers have a tapering appearance, 
due to tumefaction of the interphalangeal joints. There is ischemia of the right hand upon 
slightest elevation, reactionary rubor in the pendent position. 

The right radial and ulnar pulses are imperceptible; also the right brachial below the 
first inch of its course. 

The pulses of the left upper extremity are present; no evidence of any disturbance in the 
lower extremities. 

Pathogensis. —It is believed that arteritis may result from 3 different 
causes; firstly, from the bacteria which have caused the primary malady 
(acute infectious disease); secondly, from a secondary invader; or thirdly, 
through the effects of toxins. The bacteria which are believed to be com¬ 
monly responsible for arteritis are the typhoid bacillus, the pneumococcus, 
and streptococcus. Often a secondary invader is said to provoke the lesions. 
Those who lay stress upon the effects of toxins on the arteries mention the 
lesions in the smaller vessels (arterioles of the viscera) as examples. 

It has been a mooted question as to whether infection of arteries takes 
place by way of the vasa vasorum, the lymphatics, or directly through con¬ 
tact with the streaming blood. A review of the work of Wiesel and others, 
and a study of the material in the case of Kramer, would lead to the conclu¬ 
sion that at least in some of the cases of acute arterial disease complicating 
acute general infection, focal necroses attributable to impaired circulation in 
the arterial wall itself, or embolic processes in the vasa vasorum must be 
responsible. A reference to Fig. 149 will show the extent of the necrosis 
in the artery, the reaction immediately about it in the adjoining arterial wall, 
and the intact condition of the internal elastic membrane. Here an embolic 
agent whose portal of entry is through the vasa vasorum seems to offer the 
most plausible explanation of the degenerative lesion. 


TUBERCULOSIS OF THE ARTERIES 


455 


CHAPTER LXXVII 

TUBERCULOSIS OF THE ARTERIES 

Two distinct forms are recognized. In one the arteries are involved by 
propagation from the vicinity (secondarily); in the other they are the seat 
of embolic, or metastatic infection from a distance. 

The first of these need not be discussed here, since it does not concern 
the vascular derangements of the extremities. It will suffice to point out 
that the arteries are involved in the tuberculous process in all chronic tuber¬ 
culous foci. 

As for the second type, it has been shown 1 that the following arteries 
may be thus affected: the meningeal, the renal, the pulmonary artery, 
the aorta, the brachial and subclavian, the iliac and the. femoral. The 
tuberculous inflammatory processes in the arteries occur in the form of 
periarteritis and endarteritis. 



Fig. 150.—Tuberculous periarteritis and aneurysm of pulmonary artery. A, Afferent 
artery B, efferent artery; C, lumen of the aneurysm, a, Media; b, internal elastic lamina; 
Ct external elastic lamina; d, diffuse proliferation of intima; e, margin of point of arrosion 
of media; /, margin of point of arrosion of elastica externa; h, proliferation m intima, 1, 
aneurysmal dilatation of the hyalin intima; j, cheesy masses. {Benda) 

Periarteritis is noteworthy in the arteries of all tuberculous foci. A 
concomitant proliferation of the intima leads to narrowing that is sometimes 
followed by thrombosis and obliteration of the lumina. The inflammatory 
process advances from the adventitia through all the layers to the intima, 
and is accompanied by leucocytic and lymphocytic infiltration. 

1 Orth, Marchand, Weigert, quoted by Roger and Gouget, Maladies des Arteres, 
Bailliere, 1915, p. 143- 



456 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In this way the arteries are converted into solid cords that resist the tuberculous degen¬ 
eration for a long time. When end arteries are affected, nutritive disturbances of the organs 
supplied by them occur. So, in the brain, anemic foci with softening may result from 
tuberculous periarteritis. More rarely, when larger vessels are involved, the tuberculous 
periarteritis may penetrate into the lumen, causing local or general dissemination of 
bacilli, as in the kidneys. Usually, however, the inner layers of the artery become hyalin, 
may be forced to protrude by the blood pressure, forming a sort of aneurysm, and usually 
leading to perforation. This occurs in the lungs, and is the anatomical basis for lung 
hemorrhage. 

Tuberculous endarteritis is rare. It is seen in the form of solitary 
or multiple polypoid tubercles in the aorta or large arteries, either springing 
from the smooth intima, or from atheromatous foci. These polypoid masses 
are composed superficially of necrotic and thrombotic masses, whilst deeper, 
where they are attached to the intima, granulation tissue containing giant 
cells and bacilli are found. Tubercles of the intima of arteries are rarely seen 
(Fig. 150). 

Obliterative lesions are rather rare in the arteries of considerable size. 
But thromboses of pulmonary arteries are reported. And Baumler describes 
venous and subsequent arterial thrombosis occurring in both lower extremities 
in a young patient afflicted with tuberculous pleurisy. In spite of amputa¬ 
tion the patient succumbed. Histological examination showed tubercles 
in the walls of the thrombosed arteries (Menetrier). 1 


CHAPTER LXXVIII 

SYPHILITIC ARTERITIS AND GANGRENE 

There are authentic cases in the literature of gangrene of the extremities 
with primary arterial luetic lesions as the cause. It is not always easy to 
glean accurately from the perusal of recorded cases as to whether gangrene is 
due to primary acute, or to slow, obstructive changes in the vessels, to second¬ 
ary thrombosis, or to recrudescing luetic involvement of collateral paths in 
cases in which circulatory impairment has already been present for some time. 
However, an exposition of the facts at our disposal with a description of the 
various arterial lesions is important for an understanding of our theme. 

Pathology. —The smallest arteries participate in every gummatous 
inflammation to such an extent that in all probability, the typical necroses 
are rather the result of nutritive disturbances due to arterial lesions, than to 
the action of specific toxins. The smallest vessels may show complete closure 
of their lumina, and various degrees of encroachment upon their patency due 
to thickening of the intima. Cellular infiltration of the adventitia usually 
accompanies an intact media. 

In the small arteries there is an absence of those calcareous deposits and 
macroscopic necroses seen in arteriosclerosis. In recent cases the inflammation 
involves the adventitia only. Here there are foci of small cell infiltration, 
usually lymphocytic, with occasional leukocytes. Sometimes the latter are 
present in large numbers, particularly about areas of necrosis at the boundary 
of the media. The intima is very intensively diseased. Some of the 
thickening of the intima is doubtless due to a compensatory regenerative 

1 Menetrier, Arch, de med. exper., 1890. Cit. by Roger and Gouget. 


SYPHILITIC ARTERITIS AND GANGRENE 


457 


proliferation. With this, there may be thrombosis. In severe cases the 
small cell infiltration may be associated with giant cells and necrosis, involv¬ 
ing the whole of the vessel’s circumference. The media is relatively more 
resistant, and may be partly free at a time when the intima already shows 
gummatous foci, and leucocytic infiltration. The lumen becomes closed 
through intima proliferation (Fig. 151), and partly through thrombosis. 
With the infiltration of the intima, there is interruption in the elastic 
lamina that are destroyed in a passive manner, and do not proliferate as in 
atherosclerosis . 


Fig. 15i.—-G ummatous panarteritis (cerebral); a, adventitia in media with large gum¬ 
matous infiltration; at b, giant cells; c, internal elastica, lamina split by gummatous infiltra¬ 
tion into several lamellae; d, perforation of elastica; e, compensatory proliferation of intima; 
/, small gummatous infiltration of intima. {Benda) 



During the healing process, the cellular infiltration of adventitia and 
media disappears, and the intima proliferation shows connective tissue 
replacement. New formation of elastic tissue may then follow. 

The features are, therefore, first, cellular and gummatous infiltration 
with or without necrosis; second, destruction of the elastic lamellae; third, 
giant cell formation near the internal elastic lamina; fourth, giant cells out¬ 
side of the vessel wall; fifth, proliferation of the intima; and sixth, secondary 
thrombosis (Figs. 151 and 152). 

If we compare these findings with those in thrombo-angiitis obliterans, we 
will note that the striking differences are the presence here of giant 
cells outside of the vessels, the destruction of the elastic tissue, the prolifera¬ 
tion of the intima, the foci of gummatous infiltration, the necroses of portions 
of the vessel wall, and the type of thrombotic organization. 

According to Rosset 1 the lesions of syphilitic polyarteritis vary con¬ 
siderably, the arteries being sometimes converted into hard cords, sometimes 

1 These de Paris, 1920. 


458 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


calcareous. The caliber of the artery may be simply narrowed, the lumen 
remaining more or less circular. Or there is a parietal endarteritis, the lumen 
of the vessel being deformed. In certain sections complete obliteration has 
been observed, due either to hyperplasia of the walls, or to thrombosis at the 
level of a plaque of arteritis. Above the point of stenosis, the caliber of the 
artery may be augmented; the narrowings may be few, or multiple over long 
stretches of the vessel. In the stenosed areas lesions may be absent or 
minimal; or occasionally there may be slight dilatation. 

Microscopically the intima is particularly involved, the external and 
middle coats being relatively intact. The subendothelial coat is 4 or 5 



Fig. 152.—Recent gummatous periarteritis (cerebral); a, intima proliferation; b, 
inflammatory infiltration in the outer margin of the intima with a giant cell; c, elastic 
limiting lamella interrupted by leukocytic infiltration; d, media with small foci of leuko¬ 
cytes; e, adventitia with large gummatous infiltration; at/, necrosis. {Benda) 

times the normal size, thickened by virtue of concentric layers of numerous 
fixed connective tissue cells. The internal limiting elastic membrane is inter¬ 
rupted in a number of places by new formed tissue of vascular type, 
originating in the media. The intima presents protuberances due to rounded 
vegetation, which may project into the lumen. 

The media shows very little although the muscular tissue may be atrophied. 
The adventitia is thickened, and there is distinct periarteritis that may 
extend to the accompanying veins. 

The lumen of the vessel may be obstructed by clots which show various 
stages of organization. 

Druelle divides the lesions into 3 types. The first is one in which there 
is a panarteritis with all of the arterial coats involved. It may be acute, and 
offer a fulminating clinical picture; or chronic, when it constitutes the ana¬ 
tomic substratum for ectasis and syphilitic aneurysm. The second type 
shows the lesions of endarteritis. This process is said to lead to sclerosis, 
but not to gummata. As a result, narrowing and even obliteration of vessels 
takes place, and hence, an endarteritis obliterans of sclerotic variety. The 


SYPHILITIC ARTERITIS AND GANGRENE 


459 


third is an arteritis and periarteritis with gummatous changes in which the 
alterations in the adventitia are more marked than those in the intima, both 
as regards intensity and extent. Veritable gummata appear in the arterial 
walls, and have been demonstrated in the vessels of gangrenous limbs. 
Secondary thrombosis is often an accompanying lesion that leads to the 
usual complications. It may be concluded from this exposition that in 
the first two types a positive differentiation from other arterial affections 
cannot always be made. 

Since the larger arteries of the extremities, especially the tibial, femoral 
and brachial arteries, when the seat of old luetic lesions may not offer any¬ 
thing absolutely characteristic, the following points have been suggested as 
of differential value: the predilection of the disease for certain localities 
(central nervous system); the symmetrical distribution; the circumscribed 
nature of the lesion in the vessel wall; the predominance of the proliferative 
over the regressive degenerative changes; the tendency to form nodules that 
resemble gummata; the rather rapid development of the lesions; and the 
relative youth of the patient. 

In the aorta the adventitia and media seem to be the chief localities for luetic disease. 
In the intima there is compensatory proliferation; it is involved only in the most intense 
degrees of specific infection and necrosis. In the cases of recent activity true gummata may 
be recognized. There are lentil-sized or larger yellowish necrotic foci. They can be differ¬ 
entiated from those of atherosclerosis by the gelatinous thickening of the surrounding 
adventitia, and because of the penetration of the necrosis into the adventitia. Small 
irregularities of the intima with corresponding depressions and defects of the. media are 
characteristic in the earlier stages; but later on the macroscopic diagnosis may be impossible. 
Cicatricial retraction of the intima with attenuation of the coat has been observed. How¬ 
ever, inasmuch as arteriosclerosis may show a cicatricial form, a differentiation may be well 
nigh impossible. Therefore, here again only the finding of gummatous foci, cellular infiltra¬ 
tion with necrosis and giant cells are dependable criteria for diagnosis of luetic disease. 

The finding of spirochaetae pallida in the non-gummatous form is a recent con¬ 
tribution worthy of note. Benda 1 reports the presence of numerous spirochaetes in the 
adventitia (also Strasmann 2 ). 

Incidence. —Instances of gangrene of the extremities as a consequence 
of syphilitic arteritis are of infrequent occurrence. Of 14 cases (Druelle 3 ) 
only 2 were over 50 years of age. The gangrenous process is of the dry 
variety, not unlike that of senile gangrene. As to the time that elapses 
between the onset of the syphilitic infection and the onset of evidences of 
arterial complication and gangrene, weight of opinion leans to the view that 
it is a tertiary manifestation. Nevertheless, there is a precocious form that 
appears during the secondary phase of the malady (2 years after the chancre 
in the case of Fournier). In it, gangrene is described as the sequel of an 
acute arteritis; and during this period the chancre may be still present. 
These cases belong to a fulminating or malignant precocious form of arterial 

affection. . 

Males are more frequently affected than females, there having been. 1 
female in the above series of 14- As for the lesions, the late alterations in 
the vessels need not be wholly due to syphilis, but may result from a number of 
complicating factors, amongst which those leading to atheroma, athero¬ 
sclerosis, alcoholism, and renal disease play a role. This association of 
multiple causal moments makes it often difficult to interpret the nature of the 
arterial disease. Nevertheless, certain undoubted syphilitic lesions in arteries 
have been recognized. 

1 Benda, Aschoff, Pathol. Anat., 1919, p. 86. 

2 Strasmann, Beitr. z. path. Anat., 1910, 49. 

3 Druelle, These de Paris, 1906. 


460 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Symptomatology. —We shall discuss here merely the symptoms when 
arteries of the extremities are involved, although it must be remembered that 
intestinal forms of syphilitic arteritis are described as giving rise to painful 
crises, the analogy of intermittent claudication. Intestinal infarction with a 
clinical picture resembling that of mesenteric thrombosis has been reported. 

There are very few, if any, distinctive features that will differentiate the 
symptoms brought on by syphilitic disease of the vessels of the extremities 
from occlusive lesions due to other causes, such as atherosclerosis or thrombo¬ 
angiitis obliterans. 

The onset may be insidious and progressive, with weakness and heaviness 
of the affected extremity. The sensations of cold, formication and vague 
pains are described. Or the onset is sudden with severe violent pain in 
the lower extremities, causing the patients to stop in their walk. The 
affected limb may become livid, and the pulsations feeble. This picture 
is comparable with that described elsewhere as due to sudden thrombosis in 
arteriosclerosis and thrombo-angiitis obliterans. 

At the beginning the dominant symptom is pain which may be lancinating, 
prevent sleep, even necessitating injections of morphine. Whilst this 
pain may be diffuse at first, it is apt to be localized in the neighborhood of 
one of the toes later on, particularly when trophic ulcers or wounds appear. 

Discoloration of the skin of the foot or hand has been described as not 
unlike the erythromelia of thrombo-angiitis obliterans, or a livid tint may 
predominate. The pulsation in the affected vessel or beyond the site of 
obstruction disappears. Sensory disturbances have been reported, such 
as hyperesthesia, and anaesthesia. Ischemia is not infrequent, and may 
possibly be elicited on elevation of the extremity. 

Improvement in symptoms may occur spontaneously or after treatment. 
Without treatment, however, the condition gradually becomes worse and 
gangrene may appear after months or lapse of years. The gangrene is usually 
sudden in its appearance and progressive. With it pain becomes excru¬ 
ciating. In most cases a patch of dry gangrene appears in the neighborhood 
of a toe. Usually this gangrene is limited to one or more toes, but may extend 
for a variable distance. 

Some of the French authors describe a special form with intermittent 
claudication, although careful anamnestic data would probably reveal that 
this symptom is common to many of the cases. Crises of intermittent claudi¬ 
cation with exceptional pallor of the extremities also occur. 

The affected arteries may be tender to touch, their pulsations reduced. 
With the more rapid development of lesions, with or without thrombosis, 
there may develop sudden pain in the calf of the leg followed by paresthesia 
and numbness. The pain is aggravated by motion, often increased at night. 
At the same time the extremity becomes colder and pale, and the symptoms 
may gradually abate. Or, the symptoms may give way to those of impend¬ 
ing or of well developed gangrene. 

Clinical Forms. —A survey of the literature permits of the following 
grouping of cases, which, however, must not be accepted as having any further 
value than for purposes of clinical orientation. 

First, syphilitic arteritis of the lower extremities with clinical picture 
of intermittent claudication. 

Second, simultaneous clinical involvement of the arteries of the upper 
and lower extremities. 

Third, associated lesions of the intestinal arteries. 

Fourth, lesions of all the vessels of the lower extremities. 


SYPHILITIC ARTERITIS AND GANGRENE 


461 


Fifth, lesions of the digital arteries alone with benign course (gangrene 
of digits). 

A clinical grouping given by other authors includes a subacute and an 
acute variety. 

1. The Slow or Progressive Form. —The symptoms may or may not be 
accompanied by intermittent claudication (Druelle). 

(a) Without Intermittent Claudication. —The first symptom that directs 
the attention of the patient to the arterial affection is pain of variable intensity 
along the course of one of the known arteries of the limb. This develops 
slowly and is aggravated by pressure and movement of the affected extremity. 
The artery may be converted into a tender and hard cord. The respective 
pulsations are diminished, and the circulation may be impaired in the distal 
parts, the skin being pale, cold, or even livid. With treatment, however, and 
rest, the circulation may be restored, but recurrences are possible. Of the 
other sensory disturbances, there may be formication and other paresthesiae, 
or even anaesthesia. Later disturbances in motility and even contractures 
may supervene; trophic disturbances are also reported. After administra¬ 
tion of mercury all of these symptoms may diminish and even disappear. 

If treatment is not instituted, gangrene may result. This is usually 
of the dry type, may be limited to the toes or the fingers, but may involve the 
larger part of an extremity. 

(, b ) Cases with Intermittent Claudication. —It is not quite clear why some of 
the authors emphasize the occurrence of this as a separate form; for it has 
been shown that this complex may obtain in all the varieties of obstructive 
arterial affection of the extremities. Possibly its significance has been 
emphasized because it may be a prominent feature in young individuals 
previously healthy, when attacked with syphilitic lesions of the vessels. 

2. Acute Form. —The most characteristic symptom is pain, which is 
often intense, indeed, so excruciating that the patient constantly seeks to 
alter the position of the limb in the hope of obtaining relief. Some even 
pray for amputation because of their suffering. 1 Other severe symptoms 
are associated. The limb may become cold, have a cadaveric appearance, 
and even the sensations of certain parts of the limb may become abolished. 
In this acute form the French authors speak of painful anesthesia , which 
means an association of pain and an anesthesia of the part. With it the 
motile functions are in abeyance. The skin may become livid and morti¬ 
fication may set in. 

Examination reveals the disappearance of the pedal pulses, posterior 
tibial, popliteal and even the femoral. In these types the gangrene may be 
more extensive than in the slow forms, and when it begins in the toes, may 
rapidly extend so as to invade a large part of the leg. 

3. A recurring form of gangrene due to syphilitic arteritis is reported. In 
its clinical course this closely resembles that of thrombo-angiitis obliterans. 

4. Syphilitic Arteritis in Advanced Age. —Patients, who by reason of their 
age, may be expected to present arteriosclerotic changes may, when lues is 
present, present a pathological and clinical picture hard to interpret from 
the etiologic standpoint. 

1 Compare with similar cases of acute thrombo-angiitis (Chap. XLI). 


462 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER LXXIX 

PERIARTERITIS NODOSA 

This is a rather rare disease (about 52 cases reported in the literature), 
and was first described by Kussmaul and Maier. 1 The characteristic lesion 
is an exudative inflammation of the periadventitial structures, the adventitia, 
the media, and sometimes the intima. By virtue of necrosis of the media, 
both true and false aneurysms with thrombosis (sometimes with hemorrhagic 



Fig. 153.—Periarteritis nodosa, a, Thrombus containing leucocytes in the lumen; 
b, internal elastica interrupted through inflammatory process; c, media; d, fresh process of 
degeneration; e, large focus of degeneration; /, inflammatory infiltration of media; g, 
external elastic coat with numerous interruptions; h, adventitia with leucocytic infiltration. 
( Benda) 

extravasation) may develop. These lesions usually effect varying degrees 
of injuries to the area supplied by the arteries, such as infarction and coagu¬ 
lation necrosis. Later, proliferative adventitial or intimal changes, reparative 
or organization processes may take place. The name was given because 
of the presence of so-called nodules formed by multiple thrombosed 
aneurysms often arising from vessels of small size. 

The important lesions in this disease are the necroses and the hemorrhages of the media, 
the inflammatory (leucocytic) infiltrations of all three layers with the associated thromboses 
in the lumen (Fig 153), and the aneurysms, which alterations may occur in numerous discrete 
foci. The lesions tend to healing with connective tissue cicatrization of the mural changes, 
with proliferation of the intima and resulting obliterating endarteritis; or, with organization 
of thrombi (Fig 154). 

1 Kussmaul and Maier, Deutsch. Arch. f. klin. Med., 1366, I, 484. 


PERIARTERITIS NODOSA 


463 


Clinical Manifestations. —Depending upon the seat of the arterial 
lesion, cardiac, pulmonary, renal, intestinal, cerebral, abdominal, and 
manifestations in the extremities, are the chief features of the symptoma¬ 
tology. Detailed accounts will be found in articles by Lamb 1 and Klotz. 2 
Here we are concerned only with those data that the literature offers as 
referable to involvement of the arteries of the extremities. 



Fig. 154. —Periarteritis nodosa in a branch of the superior mesenteric artery with 
recent organization of thrombus, a, Adventitia; b, cicatrization of inflammatory focus, 
c, external elastic lamina; at d, interruption of the elastica by cicatricial tissue; e, media, 
at /, interruption by cicatricial tissue; g, internal elastic lamina; at h, the latter is inter¬ 
rupted; i, granulation tissue in the intima with new vessels (fe); l, mass of thrombosis. 
{Benda) 

Manifestations in Extremities .—Pain and cramp-like sensations have been 
described. Where the subcutaneous vessels have shown specific patho¬ 
logical changes, pain and nodule formation in the areas involved have been 
demonstrated. When the latter are present, extirpation of a nodule and 
pathological examination may lead to correct diagnosis. 

Pains in the voluntary muscles and along the peripheral nerves are a 
feature and may be so pronounced as to be diagnosticated as neuritis, 
poliomyositis or trichinosis. 

1 Lamb, Arch. Int. Med., 1914? * 4 , 481. 

2 Klotz, Jour. Med. Res., 1917, 37 , No. 1, p. 1. 


464 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER LXXX 

SYPHILITIC DISEASE OF THE VEINS 

Only those lesions will be described here that may give a picture of migrat¬ 
ing phlebitis that could be mistaken for similar phenomena in thrombo¬ 
angiitis obliterans. 

The lesions of syphilitic phlebitis should be recognized and differentiated 
from other forms especially from thrombo-angiitis obliterans. Indeed, 
certain histologic similarities may require the following exposition for 
clarification. 

Clinical Characteristics. —The veins of the extremities, particularly those 
of the lower extremities, are usually affected. In rare cases, phlebitis has been 
observed in the face. Frieboes 1 has reported 2 such cases. In 1 of these, 
there appeared during the secondary stage, bilateral cord-like indurated areas 
1 3 ^ to 2 cm. in length, and of the thickness of a lead pencil. These were situ¬ 
ated in the temporal region just adjacent to the eye, causing some slight promi¬ 
nence of the overlying skin. Under antisyphilitic therapy these disappeared. 
In a second case, similar cord-like manifestations appeared along the course 
of the vessel, just under the skin in both temporal regions, due to inflamma¬ 
tory processes in the veins. 

According to some authors the veins may be involved so gradually that 
careful palpation is necessary to elicit pain along the venous cords. However, 
the attention of the patient may be drawn to the part by a sensation of dis¬ 
comfort, a tenderness of the affected limb, or, muscular cramps at night, and 
formication. 

The seat of the phlebitis is usually one of the superficial veins of the 
extremities, such as the internal saphenous. On inspection one finds the 
affected limb normal in volume, with sometimes a slight rosy discoloration 
of the overlying skin, the discolored area has about the width of one finger. 
The venous cord is indurated, varying in size from a quill to a lead pencil, 
usually not adherent to the skin at first. Three varieties have been described: 
first, partial, syphilitic phlebitis; second, segmentary; and third, total. This 
grouping depends upon whether the lesion is limited to a portion of the vein, 
its course over a segment of the limb, or its total length. Sometimes slight 
edema is present in the region of the involved vein. 

The clinical course is a rapid onset with inflammatory symptoms, then 
a gradual decline, leaving an indurated cord under the skin. All manifesta¬ 
tions disappear within 4-6 weeks. Embolism is very rare in the course of 
syphilitic phlebitis. In some cases recurrences have been observed, various 
veins being successively involved. 

When the deep veins are involved the clinical picture may be that of 
milk-leg, but both veins of the upper and lower extremities may be affected. 
It is rare for but one vein to be involved, a multiplicity of venous lesions being 
the rule. 

Pathology.— Descriptions of the histologic chaijges vary greatly in the 
literature. The striking pictures observed by some are produced by the 
presence of foci containing giant cells and nodules in the perivascular tissue, 
suggestive of miliary tubercles. According to other authors, such lesions 


1 Frieboes, Dermat. Ztschr., 1913, 20, 125. 


SYPHILITIC DISEASE OF THE VEINS 


465 


have not been seen, and the alterations are confined to the vessel itself with 
the production of a clot without any recognizable, specific, architectural 
changes. It would seem, therefore, that for differentiation from thrombo¬ 
angiitis obliterans only those observations in which giant cells are a feature 
need special mention. 

In most cases red thrombosis was observable, the lumen being more or 
less completely filled with a clot. According to Roques the intima is altered, 
being replaced by tissue made up of round cells, fusiform cells, and a deposi¬ 
tion of connective tissue. This new formed tissue produces thickening of 
varying degrees. 

The internal elastica is well preserved, a solution of continuity being 
present only in a few places. 

The other coats contain a large number of cells of variable shape, some 
round, others fusiform or elongated. Giant cells were absent. 

Spirochaetae pallida have been demonstrated in the vein walls by Ravaut 
and Ponselle. 1 



p IG> l55> —Syphilitic lesions of the vessels and perivascular tissue in phlebitic nodule 
removed from veins; obliterating proliferative lesion seen in larger vein on the right; on the 
left, a small vein is infiltrated, its elastica conserved; below and above, syphilitic miliary 
tubercle-like nodules with giant cells. ( Frieboes ) 

Specimens were extirpated by Frieboes and the lesions found may be 
described as (i) of the perivascular tissues, and (2) of the vessels themselves. 

A characteristic and distinguishing feature contrasted with thrombo¬ 
angiitis obliterans, is the inflammatory lesion outside of the vascular domain. 
These lesions have been variously described, but the presence of giant cells 
of the Langhans type associated with endothelioid plasma and mononuclear 
cells makes a picture that is not found in the extravascular tissues in thrombo¬ 
angiitis obliterans. Frieboes describes an inflammatory lesion composed 
of an infiltrate of epithelioid, mononuclear, and. plasma cells, associated 
1 Ravaut and Ponselle, Soc. Med. des Hopitaux, Jan. 12, 1906. 


30 


466 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


with destructive lesions of the connective tissue fibers and degeneration of 
capillaries. There are also foci or conglomerates of such cells and occasional 
giant cells of the Langhans type. Some of the nodules in the connective 
tissue composed of endothelioid, mononuclear and giant cells are suggestive 
of tuberculosis. 

The smaller vessels in the connective tissue show an arteritis obliterans 
with degeneration of the whole vessel by reason of reactive processes. There 
is an intense proliferation of the intima of the small vessels, almost occluding 
their lumina. 

In the larger veins the media is infiltrated with cells, the elastic fibers being displaced 
and spread apart and fragmented. With this change, the lumen of the vessel becomes 
eccentrically displaced. The process is one of vascular destruction by reason of new formed 
inflammatory tissue. The proliferating cells constituting the latter replace the vascular 
wall, so that in places nothing but a few elastic fibers remain, as shadows of the inflamed 
vessel; or, a few concentrically placed cellular groups within elastic fibers may be the only 
remnant of a vessel (destructive lesion). 

In another case the infiltrate was found especially confined to the neighborhood of the 
vessels, occasional giant cells being interspersed here and there, amongst the new formed 
perivascular elements. 

0 



Fig. 156.—destructive inflammatory lesion of syphilitic nature in a vein. The 
elastica is destroyed; below, the lumen of the vessel is occupied by new formed vessels, 
giant cells, endothelioid and plasma cells. ( Frieboes ) 

The vascular changes in the second case of Frieboes showed all transitions 
from early endothelioid proliferation within the vessel, up to complete 
destruction. 

In Fig. 155 the wall is seen infiltrated with cells causing encroachment 
upon the lumen and remarkable enlargement of the total diameter of the 
vascular section. The elastic fibers are separated, split, torn and displaced. 
On the left in the picture there is a small vein in which the elastic ring is still 
conserved, but the lumen is filled with proliferating endothelium. Below 
in the picture there are nodules composed of proliferating cells and giant 
cells. These are the foci suggestive of miliary tubercles. 


SYPHILITIC DISEASE OF THE VEINS 


467 


Fig. 156 shows clearly the destruction of the elastic ring, and the lumen 
contains endothelioid cells, mononuclear and giant cells and new formed 
vessels. 

In short, the aforementioned lesions differ from those of thrombo-angiitis 
obliterans, in that foci of syphilitic inflammatory lesions are present in the 
tissues outside of the vessels; secondly, in that they are of exquisitely pro¬ 
ductive nature with a tendency to cause destruction of the vessels. This 
is accomplished through the action on the elastic and connective tissue 
elements; and finally, complete obliteration of the lumen by new formed 
tissue with or without thrombosis may be the significant intravascular lesion. 



Fig. 157.—Inflammatory infiltration in the media of a vein in secondary syphilis. 
The cells are mostly of the plasma cell type with some endothelioid proliferation and round 
cell infiltration. ( Hofmann ) 


The inflammatory changes in the veins vary according to the literature. 
Those described by Hofmann 1 resemble those of thrombo-angiitis obliterans 
so closely that the points of differentiation are worthy of note. There are 
enough differences in the histologic picture of the two lesions to enable the 
microscopist to make a distinction. 

A thrombotic and inflammatory lesion is present in the veins (Hofmann). 
The presence of giant cells we believe might lead to confusion in differentiation 
from lesions of thrombo-angiitis obliterans. 

The inflammatory infiltration of the wall of the vessel differs from that of 
thrombo-angiitis obliterans in that the predominating cells are plasma cells, 
particularly grouped about the vasa vasorum. Besides this, the media is 
the seat of marked proliferation of the fixed cells, and of round-cell collections 
(Fig. 157). Just under the elastica interna there is an intensive inflamma- 

1 Hofmann, Arch. f. Dermat. u. Syph., 1905, 73, p. 245. 



468 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


tory lesion represented by proliferation of endothelioid cells, fixed connective 
tissue cells, collections of plasma cells, together with occasional giant cells. 

This localization (within the vessel wall) together with the presence of 
giant cells in this layer (Fig. 158) is characteristic of the syphilitic lesion. 
The internal elastic membrane is rarefied, displaced and destroyed in places. 

The intima shows extensive proliferation of cells of varying degrees, being 
thicker in some places than in others. Parietal thrombi are said to originate 
at points where the lesions are most intensive. 



Fig. 158.—Syphilitic lesion in vein showing giant cells in clot, and giant cells in foci 
under the internal elastic coat. ( Hofmann) 


The thrombus contains large numbers of giant cells of theLanghans type. 
In the periphery of the clot, the connective tissue fibers are developed, but 
the greater part of the thrombus is made up of red blood cells and blood 
platelets with considerable fibrin. 

Tertiary or Late Form .—The studies of Roques have shown that the deep 
veins of the upper extremity, the popliteal and posterior tibial may be 
involved. In the late stage of syphilis the multiplicity of lesions is not 
observed, and the affection seems to be less severe and more diffuse. 

The affected limb is painful and heavy, and becomes rapidly useless 
from the functional standpoint, by reason of augmentation in volume. With 
this there may be a slight elevation of temperature. 

The enlargement of the limb is striking due to edema, which may involve 
the whole of the extremity. The limb feels hard. When the edema is 
distributed about the vein, an elongated area of tumefaction is developed 
which corresponds to the course of the vessel. 

Sensory and trophic disturbances are not associated. The progress of 
the phlebitis is slow and yields to antisyphilitic treatment, the symptoms 



SYPHILITIC DISEASE OF THE VEINS 


469 


disappearing in toto in from 6-8 weeks after treatment has been instituted. 
Recurrences have not been observed. 

Histo-pathology of Tertiary Phlebitis. —The lumen of the popliteal vein in 
one case (Roques 1 ) was filled with a clot already in a state of partial organi¬ 
zation. The intima was markedly thickened, containing small rounded cells, 
and fusiform cells with new formed connective tissue. 

The other coats, the media and adventitia, contained an abundance of 
alien cells. These are regarded by this author as representing an infiltration 
with young connective tissue. 

Diagnosis of Syphilitic Phlebitis. —An indurated cord corresponding to the 
anatomical course of a superficial vein in a syphilitic when of recent origin 
must be regarded as possibly of luetic origin. The onset, however, is slow and 
insidious, and a number of veins may be affected simultaneously or consecu¬ 
tively. This type must be distinguished from a number of others, from 
thrombo-angiitis obliterans, phlebitis of rheumatism, erythema nodosum, 
nodular lymphangitis, syphilitic myositis and syphilitic gumma in a vein. 

Rheumatismal Phlebitis. —According to the French authors phlebitis of 
rheumatism is accompanied by recrudescence and exaggeration of the 
febrile phenomena and of the pain. As a rule polyarthritis is associated, or 
cardiac, pericardiac, or pleuritic lesions. The presence of syphilitic stigmata 
are of the utmost value in diagnosis. 

Erythema nodosum is easily distinguished since in a case of phlebitis the 
relation- to the vein, the mobility, the absence of adherence to the skin and 
the redness of erythema nodosum are characteristic. 

Thrombo-angiitis Obliterans. —In this disease the nodules are of two types, 
the nodules, and the cord-like swellings. In both there is marked tenderness, 
adhesion to the skin, and depending upon the situation and extent of the 
lesion, the vein is also adherent to the deeper parts. In addition, there are 
usually associated the evidences of obliteration of the deep vessels. Biopsy 
of exsected veins permits of microscopic differentiation. 

Syphilitic Gumma (Tertiary).—Here the skin and deeper parts are also 
involved. In the nodular lymphangitides the redness is striking and the 
involvement of the regional lymph node is regularly present. 

In syphilitic myositis there are also hard nodosities, somewhat elongated, 
but these can be demonstrated to lie in muscle, and are much deeper than the 
inflammatory lesions in the veins. 

In syphilitic gumma of the veins a veritable tumor is developed, that rather 
suggests a neoplasm or tuberculoma than thrombo-phlebitis. 

LITERATURE 

Weljamowitz, Mil. Med. Jour., Oct., 1898; Dermat. Ztschr., 1900, p. 136. 

Heuzard, These de Paris, 1898. 

Proksch, Uber Venensyphilis, Bonn, 1878. 

Barbe, Jour. Mai. Cut. et Syph., 1899, p. 183; France Med., 1898, p. 497 - 
Fournier et Loeper, Ann. de Dermat., 1899, p. 80. 

BondSsio, These de Paris, 1899. _ .. , 

Finger, Arch. f. Dermat., 1900, 53 > P- i°8. Verhandl. der Wien. Dermat. Gesellsch. 
Collinot, These de Paris, 1901. 

Audry et Constantin, Soc. franc, de Dermat., 12 juin, 1902, p. 321. 

Roussy, Gaz. des Hopitaux, 5 sept., 1903, p. 1013. 

Hofmann (Eric), Dermat. Ztschr., Oct., 1903, p. 470; Dermat. Ztschr., 1903, p. 540. 
Roques, These de Toulouse, 1907. 

1 Roques, These de Toulouse, 1907. 


470 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Achard et Demanche, Arch, des Mai. du Coeur, Vaisseaux, aout 1909, p. 449. 

Dieulafoy, Presse Med., 1909, p. 130. 

Etienne etLucien, Ann. de Dermat., 1909, p. 545. 

Strandberg, Verhandl. der dermat. Gesell. zu Stockholm, 22 sept., 1910; Arch. f. Dermat. 
. Nov., 1910, p. 344. 

Thibierge et Ravaut, Bull. Soc. Med. Hopit., 14 avril, 1910, p. 342. 

Balzer et Mad. Vaudet-Neveux, Bull. Soc. franc, de Dermat., 12 mai, 1910, p. 141. 
Gaillard, These de Paris, 1911. 

Torok, Pest. Med. chir. Pres., Budapest, 1912. 


CHAPTER LXXXI 

MIGRATING PHLEBITIS—MISCELLANEOUS VARIETIES 

Whilst the phlebitis of subcutaneous veins is regularly attended with 
obturating thrombosis in thrombo-angiitis obliterans and in syphilis, other 
non-thrombotic varieties have been described. 

Phlebitis Migrans with Pulmonary Tuberculosis— The following clinical 
and pathological picture is given by Schwarz. The affection involves super¬ 
ficial veins acutely with signs of inflammatory swelling, tenderness and 
redness of the overlying integument. An inflammatory process takes place 
in the vessel wall with edema and leukocytic infiltration of media and adven¬ 
titia. This is followed by the formation of new connective tissue and new 
vessels, but no thrombosis occurs. 

In short, in advanced tuberculous individuals circumscribed painful, 
inflammatory foci are found in superficial veins, the latter conserving their 
permeability. Fusiform swellings occur implicating the overlying skin. The 
acute lesions in the veins gradually give way to chronic fibrotic thickening, 
the final product being unknown since no material in this stage has been 
studied pathologically. 

Other Varieties. —There are a number of different varieties of migrating 
phlebitis usually involving the territory of the internal and external saphenous, 
the pathogenesis of which is not clear. Microscopic examination, however, 
of pieces exsected for histological researches has demonstrated, in the author’s 
experience, that the typical lesions of thrombo-angiitis obliterans are absent. 
We shall describe some of the cases that have come to our notice, giving 
clinical and pathological data. 

1. Focal Migrating Phlebitis of Unknown Origin .—In some of these a 
history of excessive smoking over many years can be obtained. In others, 
however, there are no anamnestic data that throw light upon the etiology. 
In one such case the tributaries of the saphenous were excised, and bland 
thrombi demonstrated. The media was most involved in the inflammatory 
process, the muscular fibers being separated by migrating polynuclear leu¬ 
kocytes. In some sections, foci of migrating polynuclear cells and fibrin 
were seen to penetrate the media and enter the lumen through the intima. 
The accumulation of leukocytes was most intense in this zone, although also 
present throughout the rest of the vein wall. 

C. J. R. (April 1, 1922), 33 years of age, American, had trouble in the left foot and leg 
for 8 months. This was described by the patient as a pain traveling from one place to 
another, since he did not himself detect the local changes in veins that were gradually 
taking place. 


MIGRATING PHLEBITIS—MISCELLANEOUS VARIETIES 


471 


On examination of the left leg there were several inflamed and obliterated regions in the 
course of the internal saphenous, some along the inner side of the knee and leg, others along 
the inner border of the foot, and another inflamed cord over the lower third of the thigh. 
A portion of vein about % of an inch in length in a situation in which the vein seemed 
rather acutely inflamed was excised. 

Microscopic Examination :—Lesions of thrombo phlebitis with red thrombus completely 
occluding the vein are here found, the early organization being of the bland type. There 
is an inflammatory infiltration of the vein. The fibers of the media are separated by round 
and migrating cells and edema. The inflammatory exudate does not equally involve the 
walls in annular fashion, but seems to be most pronounced over certain portions of the 
vessel wall (Fig. 159). In some sections this focal distribution of the inflammatory process 



Fig. 159.—Acute phlebitis, a portion of one of the tributaries of the internal saphenous 
vein acutely inflamed (migrating phlebitis) in a process of unknown origin (not thrombo¬ 
angiitis obliterans); diffuse leucocytic infiltration of the muscular coat and a focus of 
migrating cells located at one point where the black area is seen penetrating the intima. 

shows itself not only in the limitation of the inflammatory product to a portion of the wall, 
but also in a distinct streak-like invasion of the intima with migrating cells, in direction 
perpendicular to the circular fibers, as if a penetration of the intima and clot was thereby 
intended. In certain places intensive infiltration of the subintimal layers with inflam¬ 
matory cells can be seen extending in a longitudinal direction for a variable distance (Fig. 
160), another evidence of the focal distribution of the lesion. A similar inflammatory 
lesion can be traced for a variable distance into the tissues about the vein. 



472 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


2. Migrating Phlebitis with Infections (Non-suppurating). —Rheumatic 
phlebitis with general manifestations is referred to in Chap. LXXVI. 

3. Extensive Recurring Phlebitis. —We occasionally encounter slowly 
progressive and recurring attacks of migrating thrombophlebitis over the 
territory of the internal saphenous vein and many of its tributaries, that may 
eventually lead to venous occlusion from the foot up to the cribriform open¬ 
ing in the femoral fascia, and possibly even into the femoral vein. The few 



Fig. 160. —Inflammatory focus, wandering cells, leucocytes in the wall ol a superficial 
vein; above in the region of the intima a focus of intensive migration; throughout the main 
wall infiltration with polynuclear leucocytes. (High power of Fig. 159) 

cases observed by the author—in which thrombo-angiitis obliterans and lues 
could be excluded—were males, in one of whom a history of excessive smoking 
could be elicited. The insidious nature, the lack of exquisite tenderness and 
redness so characteristic of thrombo-angiitis obliterans, distinguish this form 
as being less intensively inflammatory. The exact etiology is unknown. 

4. Migrating phlebitis of unknown cause possibly belonging to group (1) 
has been observed in young men in whom the malady was so limited in extent 
and so devoid of marked discomfort that material for exsection and study was 
refused by the patient. One case—a physician—interpreted his affection as 
of metabolic origin, from the observation that after some recurrences it was 
arrested completely by strict dietary regime. 


CHAPTER LXXXII 

VASCULAR OCCLUSION OF DOUBTFUL ORIGIN 

It is not always possible to fathom the exact nature of the processes that 
may obliterate the arteries of the lower extremities. In our experience four 
different types of cases have presented themselves in which all of the arteries 


VASCULAR OCCLUSION OF DOUBTFUL ORIGIN 


473 


of this territory are pulseless. In two of these the diagnosis of thrombo¬ 
angiitis obliterans can be made with a fair degree of probability; in the others 
no positive conclusions as to the variety of essential lesions can be arrived at. 
Succinctly stated, these forms are: 

(1) Typical thrombo-angiitis obliterans of one lower extremity with 
absence of all the usual pulsations of the other, symptoms in the latter being 
almost nil. 

(2) Absence of all the usual pulsations of one lower extremity with a 
history suggesting an old thrombo-angiitis. 

(3) Absence of femoral and popliteal pulsations in cases in which wounds 
of the leg fail to heal, eventually necessitating amputation. 

(4) Absence of all the pulses of both lower extremities, without trophic 
disorders, and of unknown causation. 

1. We have referred elsewhere to those rare but interesting cases in which 
the diagnosis of the disease as it affects the vessels of one limb is clearly 
thrombo-angiitis obliterans, but the patient may be unaware of a similar 
process on the other side. This is due to the absence or paucity of subjective 
symptoms, but on investigation all the pulses will be found absent. 

2. Here enough anamnestic data can be elicited to warrant the belief that 
some time in the past evidences of an active or even “acute” thrombo¬ 
angiitis obliterans have been present in the limb under consideration. 

3. Not uncommonly will we encounter cases in which there is a history of 
a long state of invalidism. This is often attributed to a minor injury, acci¬ 
dental or unwittingly self-inflicted, beginning in a toe or somewhere in the 
leg, or even initiated by a minor apparently inconsequential operation done 
by a surgeon for a trifling disorder. The wound thus occasioned fails to 
heal, chronic ulceration ensues and then the patient is confined to the house 
for weeks or months. Eventually a “conservative” amputation is resorted 
to somewhere through the leg, and even this wound does not heal. Cases 
have come to the author’s notice where the stump did finally close below the 
knee and in others ablation higher up had been eventually found necessary. 

In such patients the obliteration of all of the palpable arteries was the 
fundamental cause of the local nutritional failure. One could demonstrate 
the absence of the external iliac, femoral and popliteal pulsations. Since 
all instances of this type so far observed, have had some part of the extrem¬ 
ity removed, the interpretation of the exact nature of the vascular lesions is 
difficult. The absence of intermittent claudication, previous trophic dis¬ 
orders, pain, coldness and blueness—in short, all of the usual signs of de¬ 
ranged circulation, and the latency of the affection until the infliction of the 
initiating wound—all this puts the affection into a doubtful category, one 
admitting of multiple causal interpretation. 

Thus, we may assume that any of the following pathological processes 
without clinical manifestations may account for the vascular blockage. 
(1) Luetic arterial disease; (2) atherosclerosis with insidious thrombosis, 
(3) thrombo-angiitis obliterans without symptoms; (4) bland thrombosis of 
the small peripheral vessels with ascending accretion clots (mechanical), 

(5) embolic closure without symptoms; or finally, (6) an inflammatory 
lesion (arteritis) with thrombotic obliteration of unknown variety and origin. 

If we analyze these possibilities, only the first, fourth, fifth, and sixth 
are at all likely in view of the facts and data elsewhere adduced. 

4. We shall give by way of illustration of this variety an instructive 
history of a patient in whom inability to walk and pain in both lower extremities 
from the hip down were the significant symptoms that led to the discovery 


474 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


of the ubiquitous absence of the pulses. Whether we were dealing here with 
the result of a succession of latent embolism and thrombosis, or some other 
lesion, we are at a loss to decide. 

G. G., physician, American, 43 years of age, gave the following history November 16, 
1921. The malady commenced suddenly in June, 1919, with symptoms suggesting angina 
or pulmonary embolism, the physician in charge stating that there was cyanosis of the neck 
and face at the onset, with rapid pulse and threatening collapse. Following this the patient 
was very ill for 10 days, with temperature ranging from ioo° to ioi°, with a rapid pulse, but 
with no symptoms referable to the lower extremities. 

In April, 1921, his legs suddenly gave way after a slight exertion because of sudden pain 
in both hips radiating down the legs, so that he was unable to walk. . He rapidly recovered 
from this, but ever since then the pain on exertion and the weakness in both lower extremi¬ 
ties have persisted; leukocyte count 22,000. 

November, 1921, complete status (Dr. L. Barker) revealed nothing sufficiently 
significant in explanation of the findings of vascular occlusion. 

Physical examination made by the author November, 1921, demonstrated absence of 
pulsation in both femorals and accessible portions of the external iliacs, the popliteal, 
posterior tibial and dorsalis pedis arteries. On elevation of the limbs there is very slight 
ischemia, and there is but a suggestion of rubor on allowing the legs to hang down; trophic 
disorders are absent; 17,300 leukocytes. 

In June, 1922, the patient stated that the pain in the lower extremities had diminished in 
intensity; that he had had one attack of cardiac pain which left a pericardiac sound and 
systolic murmur, and that the leukocytic count had varied from 14,000 to 18,000 since 
last November. 

In September, 1922, the patient further stated that he had had no pain in the extremities 
when at rest, but cramp-like pain on walking. On elevation of both extremities there is a 
moderate ischemia, but the color is retained in the dependent position; slight cyanosis of 
both feet, more marked in the left; both feet colder than normal; absence of all pulsations 
in both extremities from the femoral artery down. 

Epicrisis .—In the diagnostic interpretation of imperceptible pulses over 
so extensive a territory, it must be remembered that absent arterial beat is not 
exactly equivalent to occlusion. Perhaps, in cases of this sort, some arteries in 
which the pulse is extinct are still patent, and allow a small amount of blood to 
permeate, the occlusion being higher up. This assumption is a warrantable 
one, for it is based on the pathological findings in other cases in which a re¬ 
turn of pulse in the radial artery occurred after embolic closure (Chap. 
LXXXV, p. 495). 

If this view is correct, an explanation is at hand for the meager symp¬ 
tomatology in cases of this sort. 


CHAPTER LXXXIII 

MAL PERFORANT 

Our first knowledge of this disease dates back to the year 1852, when 
Nelaton 1 described an affection characterized by an indolent ulcer of the 
foot. This complication, although descriptive of a case of lepra, gave impetus 
to the study of what since has become known as mal perforant, malum 
perforans pedis , or mal plantaire perforant of Vesigne. 2 

For a correct conception of this symptom-complex—it cannot be correctly 
considered as a unity or separate malady—we must accept and comprehend 


1 Nelaton, Gaz. d. hop., Jan. 10, 1852. 

2 Vesigne, Gaz. d. hop., Feb. 5, 1852. 


MAL PERFORANT 


475 


that not only may the clinical picture vary, but also that the manifestations 
may be brought about by wholly and widely varied causes. Here we are 
confronted with a situation similar to that described under Intermittent 
Claudication (Chap. XXVI) and should more correctly view Perforating 
Ulcer of the foot as brought about by widely different causal factors. The 
literature, however, is so complete and comprehensive, and so many 
authors of note have described the condition under this name (malum 
perforans pedis), that it may be well to adhere to the nomenclature, calling 
attention to the advisability of investigating every case for the discovery 
of the underlying malady. 

Although the importance of diseased arteries has been minimized in 
this connection by a number of authors, it must be strongly emphasized that 
trophic lesions of this type may result from both obstructive arterial and 
neurogenic causes. 

Etiology.—The condition is most frequently observed in males, par¬ 
ticularly over the age of forty. The laboring and menial classes seem to be 
most frequently affected. The site of predilection corresponds with the point 
of pressure on standing and walking. Thus, the plantar surface of the foot, 
the metatarso-phalangeal joint, especially over the borders of the first and 
fifth toes, over the heel, and more rarely in the sole, are the most frequent 
sites. It is usually unilateral, but may occur simultaneously in both feet. 
The weight of opinion favors the view that a variety of fundamental affec¬ 
tions may produce the same clinical picture. 

Several theories regarding etiology have been suggested: first, the mech¬ 
anical theory; second, the vascular; third, the nervous and neurogenic 
theories; and fourth the arthropathic and osteopathic theories. 

The Mechanical Theory. —Pressure and trauma should be considered 
merely as contributory factors in determining the site of development of an 
ulcer, and not as the underlying cause. In view of the fact that perforating 
ulcers can occur in situations that are not under the influence of mechanical 
injurv, pressure or trauma, and seem to heal with the patient in bed at 
complete rest, the mechanical theory has justly lost support. 

The Vascular Theory. —Although certain authors (Hofmann 1 ) conclude 
from a study of the literature that obliteration of the arteries plays but a 
subsidiary role, the author is of the opinion that occluded arteries whether 
due to arteriosclerosis, thrombosis, or thrombo-angiitis obliterans may some 
time be followed by the development of perforating ulcers, clinically indis¬ 
tinguishable from those of less evident organic cause. Levai 2 and others are 
sponsors for the vascular theory. A careful investigation of the condition of 
the vessels of the lower extremities, including the femoral, the popliteal, the 
dorsalis pedis and posterior tibial arteries, and a search for the typical objec¬ 
tive manifestations of arterial disease, would often reveal a causal relationship 
between the vascular obturation and the trophic symptoms. 

The Nervous or Neurogenic Theory. —A number of different diseases of the 
nervous system may be attended with sensory or vasomotor paralyses or 
palsies in the territory of the lower extremities, and in consequence be asso¬ 
ciated with the appearance of trophic ulcers, of which the so-called mal per- 
for ant is a prominent and frequent example. Mal perforant may even be a 
symptom of either peripheral or central nerve lesion. 

Peripheral Nerve Lesions— The nerve lesions may be limited to the 
territory in the immediate vicinity of the ulcer, or implicate a larger part of 

1 Hofmann, Ergebn. d. Chir. u. Orth., VIII, p. 909. 

2 Levai, Deutsch. Ztschr. f. Chir., 1898, 49, 558. 


476 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the nerve distribution of the corresponding lower extremity. Peripheral 
neuritis as the result of freezing, burns, wounds, contusions and traumata of 
various kinds has been reported; so also lesions of the posterior sacral roots 
or injuries to the sciatic nerve, and tumors that involve the larger nerves or 
compress them. Other types of neuritis due to leprosy, alcoholism, lues and 
arteriosclerosis are also said to lead to the formation of trophic ulcers of the 
foot. It would appear that the anesthesia resulting from the observed lesions 
is in great part responsible for the formation of ulcers. 

Lesions of the Central Nervous System .—These are of greater importance, 
particularly tabes dorsalis. Other spinal diseases may play a role in the 



Fig. 161.—Perforating ulcers over the inner margin of the foot, second toe and outer mar¬ 
gin of the foot. ( Hofmann) 

etiology, such as fractures of the vertebrae with injuries to the spinal 
cord, tumors of the spinal cord, spina bifida aperta, or occulta, and 
syringomyelia. A few cases have been described associated with progressive 
paralysis, progressive muscular atrophy, amyotrophic lateral sclerosis, and 
spastic paraplegia. 

Certain constitutional diseases (diabetes) have been held responsible for 
mat perforant, but the pedal ulcer of diabetes does not usually belong in this 
category. The painful nature of the ulcer in diabetes is in striking contrast 
to the non-painful trophic disturbances associated with nervous disorders. 
To what extent the presence of sugar in the blood, the lesions of the 
peripheral cutaneous nerves, or the arteriosclerotic changes are participants 
in the production of trophic ulcers in diabetes is discussed elsewhere. 


MAL PERFORANT 


477 


A peripheral localized neuritis, possibly of alcoholic origin is regarded by 
Hofmann 1 as the probable cause of the occurrence of mal perforant amongst 
the menial classes of Southern Tyrol. This author observed a large number 
of cases (19) in males over 40 years of age, in whom excessive alcoholism seems 
to be the most important etiologic factor, and was attended with evidence of 
diminished sensibility in the neighborhood of the perforating ulcer. Since 
no other cause could be found, the author attempts to explain the development 
of. the trophic lesion on the basis of alcoholic peripheral neuritis possibly 
furthered by arteriosclerotic lesions. 

The Bone and Joint Theory .—The development of perforating ulcer 2 has 
been attributed to primary bone and joint lesions. 



Fig. 162.—Extensive destruction of the head of the fifth metatarsal bone corresponding to 
a callus in this region. ( Hofmann) 

Clinical Course and Symptoms— At one of the sites of predilection, over 
the sole, the ball of the big toe (Fig. 161), the outer border of the metatarsal 
phalangeal joint of the big toe, or at the heel, we are wont to observe the 
formation of a marked callus. Although this of itself is of no diagnostic 
import (since it occurs in the healthy individual), the next step in the disin¬ 
tegration of the tissues is significant. In the center of the callus, the horny 
layer becomes attenuated and some secretion begins to accumulate, lifting the 
overlying skin away and thus producing a superficial defect. The superficial 
ulcer thus formed shows little or no tendency to heal, and even though healing 

1 Hofmann, Ergebn. d. Chir. u. Orth., 1914, Bd. VIII, pp. 916-917. 

2 Levy, Ergebn. d. Chir. 11. Orth., Berlin, 1911, 2, 56; also Beitr. z. klin. Chir., 1910, 
70, H. 2 and 3. 



478 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


may take place, a recurrence is the rule. As the ulcer enlarges, it also increases 
in depth, conserving its circular external outline,, and being well demarcated 
by a wall of thickened epidermis. At first a thin watery or serous secretion 
is exuded, and putrid collections form, when secondary infection takes place. 
As a rule, this affliction is painless, and in most of the cases sensory distur¬ 
bances with diminished sensibility can be detected in the immediate vicinity. 
Where the ulcer and the surrounding parts are tender and painful, certain 
authors would rule out true mal perforant. If this view is accepted, the 
perforating ulcers associated with thrombo-angiitis obliterans, diabetes, 
and arteriosclerosis must be excluded, and only those due to neurogenic 
disturbance accepted as belonging to this category. 

Joint and Bone Lesions.—Authors are at variance as to the relationship of arthropathies 
and bony changes occurring in the immediate vicinity of perforating ulcers. There are 
some (Levy) who describe a primary causal relationship between the deep seated and 
superficial lesions, whilst there is the opposite school who contend that the bones and joints 
are merely secondarily involved. Perhaps the truth would more correctly be placed in a 
middle ground, since arthropathies may exist both independently and as a sequence of the 
trophic ulcers. 

Not infrequently, both in the neurogenic type of mal perforant, as well 
as in the deep seated ulcerative lesions associated with vascular disease, 
destruction of bones and joints occurs (Fig. 162). This would seem to be 
the rule in all the advanced cases. In at least 50 per cent, if not more, of 
the earlier cases, the corresponding joint has been found uninvolved in the 
X-ray picture. Arthropathies involving a number of articulations of the 
foot may simultaneously occur, without necessarily being associated with 
correspondingly situated ulcers. 

However, the X-ray is of exceedingly great value since the finding of 
arthropathies may call attention to the possible existence of spinal lesions. 
The X-ray examination will be particularly valuable when it discloses neuro¬ 
pathic joint changes without any definite evidences of nerve disease being 
demonstrable, but with distinct signs of local anesthesia. 

Prognosis. —This depends greatly upon the underlying nerve disorder. 
The possible complications, such as lymphangitis, erysipelas, gangrene and 
extensive infection, also the obstinacy of these lesions towards all methods of 
treatment, make the prognosis dubious. Even though pain and tenderness 
be absent, the gravity of the condition must be brought home to the patient, 
and energetic treatment applied early. 

Therapy. —This includes the care of the fundamental constitutional 
disease and the local condition, the tendency to heal depending upon the 
nature of the former. Unfortunately the basic malady is frequently not 
amenable to treatment. 

Much vaunted as of especial value are remedies such as potassium iodid 
and mercury. Of other methods may be mentioned the following: constant 
and induced electric currents, X-ray exposures, high frequency diathermy, 
and hot air. 

Because of the excellent results reported by French and Italian authors 
(Chipault, 1 Fontana 2 and Tomaselli 3 ) after nerve stretching, it may not be 
amiss to record here that the anterior tibial, peroneal, and the larger cutane¬ 
ous nerves have been exposed and forcibly stretched with a view to influen¬ 
cing the trophic condition. 

Chipault, Presse med., Sept. 11, 1895. 

2 Fontana, Riforma med., 1910, 22. 

3 Tomaselli, Gazz. d, osp., 199, 106. 


EMBOLISM AND THROMBOSIS 


479 


Local treatment should follow general surgical principles, the value of 
permanent baths (Chap. LXV) being particularly noticeable in many cases. 
Surgical procedures depend greatly upon whether there is a communication 
between the ulcer and the neighboring joint or bone. Excision of ulcers 
that do not lead to bones or joints has been found reliable in many cases. 

X-ray examination will reveal the extent of osseous involvement. When 
the latter or the contiguous joint is affected, the territory must be adequately 
cleansed by curettage, or excision of bony fragments on general surgical 
lines. When only one toe is involved and excessively so, amputation is the 
best procedure; similarly, when the metatarso-phalangeal joint is diseased. 

Whenever, by virtue of secondary infection, extensive disease of soft 
parts and bone takes place, amputation of larger parts may be advisable. 
Perhaps the Leriche operation will be of value here (see p. 525). 


CHAPTER LXXXIV 

EMBOLISM AND THROMBOSIS 

Embolism and thrombosis may be considered together, since they are 
frequently associated in the pathology of gangrene, and since it is often 
difficult to make a differential diagnosis, or to distinguish between the effects 
of the pure embolic process and the result of occlusion by thrombosis. In 
the veins only extensive thrombosis over large territories is effective in pro¬ 
ducing gangrene of an extremity or portions of an extremity, whereas, in 
the arteries, either embolism or thrombosis may lead to gangrene. 

Emboli may lodge at the bifurcation of arteries, particularly in the popli¬ 
teal or in the aorta at the division into the iliacs. The source of an embolus 
must be sought in a portion of the circulatory system, situated proximally 
to the obstructed vessel, in the left heart and rarely in the right heart, when 
the foramen ovale is patent. Emboli may be dislodged from the ulcerative 
lesions of atherosclerosis, from syphilitic arteries, from an aneurysm, or from 
arteriosclerotic, injured or infected vessels. A heart that is the seat of 
myocarditis and endocarditis or bacterial endocarditis, or that is altered in 
consequence of previous infectious diseases, such as typhus, variola, scarlet 
fever and bacteriemia (so-called pyogenic infection) may be the source of 
emboli. When the emboli contain organisms, they are called infectious 
emboli , and may give rise to metastatic abscesses. 

The cases may be divided into: (1) embolic obturation with insidious 
course; (2) thrombosis and embolism after infectious diseases, including 
pneumonia; (3) cases secondary to cardiac diseases; (4) cases following 
abdominal operations, and complicating pregnancy, in both of which the 
exact mechanism is not well understood; (5) peripheral thrombotic gangrene, 1 
or thrombotic gangrene in healthy or but slightly diseased vessels; (6) embo¬ 
lism and thrombosis complicating arteriosclerosis; (7) embolism and thrombo¬ 
sis complicating acute aortitis; and (8) embolism with aortic aneurysm. 

1 First described by the author, no reference to this type having been found in the litera¬ 
ture. However, clinical and pathological investigations have demonstrated the existence 
of this form. 


480 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


It must be remembered, however, that a discussion of these forms of 
gangrene under arbitrary categories must result in overlapping and possibly 
repetition of classes. For example, acute arteritis of infectious diseases 
may be complicated by thrombotic gangrene; and on the other hand., throm¬ 
boses occur in large arteries during acute infections where no evidence of 
arterial inflammation is discoverable. For purposes of orientation and as 
clinical aids, however, this classification is wilfully permitted. 

I. Arterial Obturation without Immediate Symptoms 

There are cases in which embolic closure of a large artery of the lower 
limbs may occur apparently without symptoms, for the patient will not 
remember having experienced anything abnormal in the affected part. 
Collateral circulation may then become so well established, that there may 
either be no subsequent symptoms at all, or such as are vaguely described 
as rheumatic or as local weakness of the affected part. Ensuing secondary 
signs may be intermittent claudication, tendency to coldness, or weakness 
of the limb, and a history of poor healing powers. Such pictures have 
developed under our own observation where one leg had been recently 
amputated for embolic gangrene. Suddenly, on careful examination, it 
is noted that the other foot becomes cold, and that the dorsalis pedis and 
posterior tibial (or even the popliteal) arteries are pulseless; 'and yet 
the patient seems unaware of any local change. Gradually, the circulation 
improves, but a certain degree of functional vascular impairment persists. 
It is in such instances that the future observer may be in doubt as to the 
nature of the cause of the vascular obliteration. 1 Vascular spasm is not 
present here, for evidences of lost pulsation persist. 

For a further discussion of gangrene complicating infectious diseases, the 
reader is referred to Chap. LXXVI on Acute Arteritis. 

The following instance of sudden arterial blockage is one that may. occur 
unbeknown to the patient in the apparently healthy limb. Here adequate 
collateral circulation compensates for the circulatory deficiency, and subse¬ 
quently effaces the symptomatology. 

I. L., male, 48 years of age (November 8,1918) suddenly developed the typical picture of 
post-pneumonic, embolic gangrene of the right foot during his period of convalescence. 

Amputation (November 13, 1918) through the mid-thigh by the author for dry gangrene 
of the foot, the proximal adjacent portion of the leg almost to the knee presenting the picture 
of moist gangrene. 

Dissection of the vessels of the ablated extremity shows that the popliteal artery was 
filled with red clots, and all of the larger veins of the leg were distended with red blood 
clots. The walls of the popliteal artery were very slightly thickened, and microscopic 
section showed some degeneration of the media. 

The initial occlusion probably occurred above the point of ablation judging from the 
nature of the clot at the point of section. This had the appearance of a “ tail 5 ’ clot (Aschoff) 
or stagnation thrombosis distal to the original point of blockage. 

Immediately after leaving the operating room and when he was brought to his bed, the 
left foot was found to be cold and cyanotic , so much so that a diagnosis of blockage of the 
proximal part of the posterior tibial artery was made. The symptoms gradually abated, 
and except for the loss of the pulses in the dorsalis pedis and posterior tibial arteries, all gross 
evidences of circulatory impairment completely disappeared. 

Embolism Without Gangrene. —Sudden blockage of the popliteal or lower 
femoral artery is not necessarily followed by gangrene. In cases with 
cardiac disease, during or after an acute infectious malady, the usual signs 
of arrested circulation in the territory supplied by the affected artery may 

1 See Chap. LXXXII. 


EMBOLISM AND THROMBOSIS 


481 


make their appearance; to wit: sudden pain in the calf of the leg or foot, 
blanching and coldness of the foot, with disappearance of the dorsalis pedis, 
posterior tibial and popliteal pulses. Through elaboration of adequate 
collateral circulation, both trophic disorders and gangrene may be averted. 

2 . Embolic and Thrombotic Gangrene after Infectious Diseases 

Gangrene complicating pneumonia may be described as a good example of 
this type. Sudden thrombosis of the femoral or popliteal artery may 
occur within a few days (four to eight) or much later (three to four weeks) 
after the onset of pneumonia. The character of the symptoms, and the 
extent of the gangrene will depend upon the site of the embolus or limits 
of the thrombosis; and the general symptoms will be determined rather by 
the general condition and disease which gave rise to the thrombotic process, 
than by the gangrene itself, subsequent emboli often causing sudden death. 

As early as six to eight days after the onset of pneumonia, or at a much 
later period, the patient will experience numbness of the foot, coldness, 
cyanosis, weakness, followed by loss of active motion, and then cyanosis of 
the distal part. On examination the dorsalis pedis, posterior tibial and 
popliteal may be found pulseless. Gangrene rapidly ensues, and, if amputa¬ 
tion is done, the femoral artery and vein are usually found filled with red clot. 

It is often difficult in these cases to determine just where the thrombus 
began, or just where the embolus became lodged. If amputation is done 
after the lapse of a week or more, beginning organization of the clot can be 
demonstrated. 

In other cases, thrombosis may occur as late as three to six weeks after the 
onset of pneumonia, beginning with sudden onset of pain in one limb, coldness 
and blanching followed by cyanosis, the peripheral arteries being pulseless. 

Clinical Course. —Either during the course of the pneumonia, or as a 
sequel, embolism or thrombosis of the iliacs, femorals, popliteals or brachial 
may occur. Symptoms of thrombosis or embolism may begin with sudden 
pain or numbness and coldness in one foot, which rapidly becomes blanched, 
later cyanotic, the dorsalis pedis, posterior tibial and popliteal pulseless. 
The typical signs of gangrene then develop, associated with distinct aggrava¬ 
tion of the general condition. Where the condition of the patient has 
allowed it, amputation was done in many of the reported cases. The mor¬ 
tality, however, has been exceedingly high, the patient often becoming deliri¬ 
ous then stuporous shortly after operation, or even before amputation was 
done. The prognosis is grave, either because of the extent of the thrombotic 
process, and the development of other emboli, or because of the menace of 
pulmonary edema and heart failure. In some instances, where amputa¬ 
tion was postponed for weeks or more, the amputated limbs revealed exten¬ 
sive organizing thrombosis of all the larger arteries and veins. 

An excellent example of gangrene of the lower extremities complicating 
pneumonia is the following. 

A. W., 30 years of age, with a history of pneumonia, and with consolidation at the right 
base, was treated at the hospital in April and May, 1914, having been discharged on theji ith 
of May. He was again admitted on the 13th day of July because of shortness of breath, 
palpitation, hacking cough with sputum. On July 25, there was sudden pain in the left leg , 
the leg being found cold and cyanotic, with pulses in the femoral, and distal to this artery 
being absent. Tenderness along the vessels could be elicited. About this time the 
patient’s mental condition changed being frequently irrational. 

July 28, the entire left foot was markedly discolored, having a purplish mottled appear¬ 
ance, the lvhole leg being cold. 

31 


482 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


August 5, the foot was edematous, swollen. The tip of the big toe was deeply cyanotic, 
the skin of the rest of the big toe was vermilion red. This discoloration appeared to be due 
to the fact that the epidermis was lifted off. Over one half of the dorsum there was a large 
bleb 4 by 3 inches probably filled with bloody serum. All the toes were intensely red, also 
due to the separation of epidermis. Over the inner aspect of the ankle there was a mild 
degree of lividity, and behind the Achilles tendon there was an enormous bleb. The red 
condition extended up to a point 4 inches above the ankle. 

In short, the early stage of moist gangrene. The leg was brawny, hard, and very tender 
to the touch, and especially hard over the calf. This did not appear to be due to superficial 
edema. 

Diagnosis. —Thrombosis of the femoral artery and vein. 

August 7, the patient was mentally confused, but rational. From now on the left leg 
passed through the various stages of gangrene. August 10, 1914, the bluish discoloration 
and patches of red and blue color seemed to be progressing upward towards the knee and 
over the outer side of the leg, the temperature of the limb being very low as far as the knee. 
The redness was still intense over the anterior half of the foot where the skin had been 
separated, and the foot had increased considerably in size. The femoral artery did not 
pulsate. 

August 12, the whole foot was cyanotic, and in an advanced stage of moist gangrene. 

August 15, the limb was much smaller, although the calf was still brawny. The whole 
leg was exceedingly cold. It presented a variegated appearance due to various changes in 
different parts of the limb. The foot had a greyish livid appearance, partly purplish and 
cyanotic. At the ankle there were patches of purple and deep red where the skin had been 
separated. The discoloration extended to the upper fourth of the leg, and was limited from 
the normal skin by a zone of purplish discoloration. The fluid having filtered out of the 
blood, the epidermis being too large, was now wrinkled over all the toes, leaving the tips of 
the toes bluish black. Evidently the whole foot is in a condition of wet gangrenp. The 
external popliteal vein could be felt as a hard cord. The right foot was edematous, prob¬ 
ably due to the impaired cardiac and renal function. 

August 24, amputation at junction of the upper and middle third of left thigh. 

August 27, very irrational, having marked hallucinations. 

September 1, some sloughing of the skin flaps. The patient was removed to another 
hospital because of his mental condition. 

_ The Gangrenous Leg. —Just before amputation the appearance of the limb was character¬ 
istic of the late stages of moist gangrene. Over the foot, the epidermis was completely 
loosened, lying in folds, torn in shreds in places, the purplish or reddish weeping cutis 
vera shining through. Higher up over the calf in the anterolateral aspect of the leg, 
there was a large patch of dry gangrene. The periphery of the gangrenous process, where 
the demarcation was taking place, showed areas of hemorrhage. (These are undoubtedly 
very similar to those which we find in early stages of gangrene.) In this process, the blood 
evidently passed through the capillaries and produced subepidermal or intra-epidermal 
ecchymoses. 

The hardness of the calf was still present, but altogether the size of the foot and the leg 
was diminished as compared with the early stages of the gangrenous process. 

At the time of operation, it was noted that the popliteal and posterior aspects of the 
thigh were very edematous, and the vessels, arteries and veins, at the point of section, were 
filled with clots, a red clot occupying the vein, a thicker clot in the periphery, with a whitish 
center in the popliteal artery. 

Dissection of the vessels showed these bound or matted together and filled with red 
clots. In places the artery was filled with a decolorized clot. Nowhere was there any well 
organized firm thrombus, such as we see in the later stages of thrombo-angiitis obliterans. 
The arteries showed a moderate amount of atherosclerosis. 

Conclusion. —A case of thrombotic gangrene or embolic gangrene probably beginning 
higher up in the femoral or in the iliac, extending rapidly down into the popliteal and poster¬ 
ior tibial. 

Microscopical Description. —The femoral artery is completely closed by a mixed clot, 
and shows no evidences of organization. The adventitia and the other layers of the 
muscularis show slight evidences of a reactive process, there being an extensive infiltration 
with small mononuclear cells, but only slight migration of polynuclear leucocytes through 
the muscularis. Here and there wandering cells have reached the internal elastic coat. 

The popliteal vein is filled with a bland clot whose periphery is being organized in the 
typical fashion. The inflammatory reaction here is less marked than in the artery, the only 
evidences being polynuclear leucocytes in the wall. Some of the small tributaries of the 
popliteal show more advanced stages of organization. 


EMBOLISM AND THROMBOSIS 


483 


Types of Gangrene. —When the edema is absent and the veins remain 
patent sufficiently long, then the characteristic picture of dry gangrene results. 
The initial coldness and pallor are also followed by blueness or bluish purple 
discoloration. Gradually the peripheral parts are depleted of their water 
content, and the tips of the toes and outer border of the foot dry up rapidly, 
gaining the characteristic appearance of the desiccated dissecting room corpse. 
The color soon changes from the dried beef appearance to a blackish brown, 
as the process extends up for a variable distance, usually almost to the ankle, 
rarely much above. 

When the condition of moist gangrene develops, because of more extensive 
thrombosis in the femoral vein, and possibly earlier thrombosis in the veins 
than in the arteries, the following picture of the local condition is typical, 
but may also be characteristic of embolic and thrombotic gangrene due to 
other causes. 

First Stage. —After a preliminary blanching which rapidly follows the 
onset of the embolism or thrombosis, the limb becomes intensely cold and 
soon develops bluish patches that give the limb a mottled appearance 
(ischemia and cyanosis). The cyanosis becomes intense, spreads rapidly; 
replacing the areas of pallor; the limb becomes livid and dusky, save for 
patches of vermilion red scattered here and there. 

Second Stage of Subepidermal Exudation. —The foot sometimes becomes 
edematous, the calf brawny and hard, and extremely tender; the soles are 
livid or they show a striking vermilion red. Over the dorsum of the foot, 
large blebs or bullae form, which contain bloody serum, and some of the 
toes may become intensely red, because of the separation of the epidermis, 
the weeping cutis vera shining through. The red condition of the foot extends 
up for a variable distance to the ankle, or even higher, giving the limb an 
angry red appearance, characteristic of the second stage of moist gangrene. 
When edema precedes the gangrene, the brawny and swollen condition of the 
limb may be intense. 

Third Stage of Intense Lividity. —As the gangrenous process becomes 
more advanced, the bullae become larger; the epidermis hangs in folds, 
breaks and allows the serum to escape. The color of the skin changes to a 
deep purple, except for places where the weeping cutis vera still shines 
through. The general color is often a grayish purple, because of the combina¬ 
tion of the dead epidermis and the bluish red cutis vera. Associated with 
these typical signs of moist gangrene there may be patches of dry gangrene. 
Higher up, at the periphery of the gangrenous process, where demarcation 
begins to take place, there are usually areas of hemorrhage, or ecchymosis. 
The limb above this line is indurated, tender, and usually much enlarged. 
Sometimes the external popliteal vein can be felt as a hard cord. The 
popliteal and the femoral are frequently pulseless. 

The final stage of disintegration has been previously described. 

Pathology.— Although it has not been possible in the author’s experience 
to demonstrate the relationship between arteritis and the thrombotic 
processes in the larger arteries (femoral, popliteal) leading to gangrene m 
pneumonia, a number of authors describe such acute arteritis as a complica¬ 
tion of this malady. Head 1 mentions three cases in which gangrene followed 
after resolution in pneumonia, and according to the literature, an arteritis 
was supposed to have existed. In one of these, where a clot was found 
lodged in the femoral artery, the pathological report described multiple 
round cell infiltration in the adventitia of the femoral artery. 

1 Head, Am. Jour. Med. Sc., 1921, 162, p. 157. 


484 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


On dissection of limbs (of pneumonic cases) the vessels are found matted 
together by intense edema and infiltration. The posterior tibial and femoral 
arteries are filled with red clot, decolorized in places, but nowhere show¬ 
ing advanced organization, even when the limb is removed eighteen to 
twenty days after the onset of the thrombosis. Histological examina¬ 
tion of such vessels shows a bland clot undergoing early stages of organi¬ 
zation. The peripheral layers of the muscle, of the media and the adventitia 
show extensive infiltration with mononuclear cells. No definite data as 
to the cause of the thrombosis can be learned from the study of the vessels 
unless they can be obtained within a few hours after embolism or throm¬ 
bosis has occurred. In the later stages, the usual signs of organization 
are present, the organizing process being often older in the veins in the cases 
of moist gangrene. 

In one of the cases of post-pneumonic gangrene described, where dissection 
was made by the author, vessels of the amputated leg revealed the following: 
The large vessels (femoral and popliteal) were matted in their sheaths 
surrounded by considerable edema everywhere filled with red clots. Some of 
these were found decolorized in places, but nowhere were they firm, nor did 
they suggest the picture of thrombo-angiitis. The femoral, popliteal and 
posterior tibial showed these changes. Recent thrombosis was found in 
other vessels situated distally. Macroscopically one could have concluded 
that here was a case of either thrombotic or embolic gangrene with the 
vascular occlusive lesion probably beginning in the femoral or possibly in the 
external iliac artery, with thrombosis extending rapidly downward. 

Histological examination of the femoral and popliteal arteries showed the 
following lesions: The lumina of the arteries were filled with clots. The 
adventitia and media were infiltrated with mononuclear cells interspersed here 
and there by a moderate invasion with migrated leucocytes. The veins, 
too, revealed similar changes with some organization of the clots. 

All these changes could be regarded as being secondary to, rather than as responsible for, 
the occlusive thrombosis, for the cite of the initial lesion cannot be determined in the limited 
vascular territory obtained by amputation. 

Gangrene with Other Infections. —Rolleston reported a case in which a 
lower extremity was thus affected in a case of diphtheria. He could find 
but one reported in which an upper limb was involved. 

Thrombosis in veins (with phlebitis) has been described as an important 
and relatively frequent sequela of influenza . 1 It is peculiar that both veins of 
the lower and upper extremities are frequently affected (brachial and axillary). 
The onset may be very acute and rapidly progressive. The process may be 
bilateral in large venous channels and may lead to gangrene. 

Occasionally venous thromboses of the arm and leg veins may be associ¬ 
ated and complicated with gangrene of the foot. 2 Almost all the veins of the 
limb may become thrombosed. Closure of one popliteal artery, or of both 
iliac, femoral, or popliteal arteries with symmetrical gangrene has been 
described. 3 Orth 4 has reported a case of symmetrical gangrene due to throm¬ 
bosis of both popliteal arteries; also a case of gangrene of the distal phalanges 

1 Leichtenstern, Deutsch. med. Wchnschr., 1890, Nos. 11, 15 and 18; also Spez. Path, u 
Therap. (v. Nothnagel, 4, Wien). 

2 Johannsen, St. Petersb. med. Wchnschr., 1890, No. 46. 

3 Friederich, Die Influenza Epidemie, etc., Arbeit, a. d. k. Gsndhtsamte, 1894, 9, Berlin. 

4 Orth, Deutsch. med. Wchnschr., 1918, No. 47, p. 1298. 


EMBOLIC GANGRENE 485 

of all the fingers of one hand. A more detailed account of this subject will 
be found under Acute Arteritis (Chap. LXXVI). 

Embolic gangrene complicating chorea was observed by Chodak. 1 

V. H., aged 12 years, was admitted into the Royal Free Hospital on December 7, 1918, 
suffering from chorea of a week’s duration. This was a first attack, and there was no pre¬ 
vious history of rheumatism; no history of shock or overwork. Two years previously she 
had had diphtheria, with a bad attack of tonsillitis during convalescence. The mother 
had had rheumatism and one sister has had chorea. On admission the patient, a thin slip 
of a girl, was found to be suffering from a moderately severe attack of chorea, all parts of the 
body being affected. There was very little loss of strength on the left side, but the right 
hand grip was poor and feebly sustained. All reflexes were exaggerated. 

Ten days after admission the right hand began to go white, the finger-nails blue, though 
the hand did not actually feel cold to the touch. The onset may be described as rapid 
rather than sudden, and it was fully a week before gangrene of the finger-tips and ball of the 
thumb had definitely set in. During this time the pallor spread up the forearm. There 
was no pulse at the wrist, but the brachial could be felt pulsating about half way down the 
upper arm, and after a time there was distinct pulsation of the superior profunda artery. 

The temperature throughout never rose above 99 0 F. and was rarely as high as that. 
Later still, the brachial pulse slowly disappeared, and the brachial artery could be felt like a 
thick cord along the arm. 

The little finger recovered, and lines of demarcation gradually formed on the remaining 
fingers. The ball of the thumb appeared at first to have escaped as the discolored skin 
peeled away from it, but there must have been considerable damage to the muscle, followed 
by contraction of the scar tissue, which has led to considerable deformity of the thumb. 

It was the consensus of opinion of those to whom this case was presented 
that it was due to embolic gangrene. 

Puerperal Gangrene. —Under this appellation quite a number of authors 
have described gangrene of the extremities complicating pregnancy. Of 
76 cases, 2 53 involved the lower extremities, 10 the upper. Arterial obstruc¬ 
tion through embolism or thrombosis is given as the cause in 29 cases. 


CHAPTER LXXXV 

EMBOLIC GANGRENE—CONTINUED 

3. Embolic Gangrene with Cardiac Disease 

When this occurs in young and middle-aged individuals, the source of 
the embolus is usually the left heart. Autopsy not infrequently reveals 
thrombi in the left auricle as the probable source, or chronic endocarditis 
with valvular lesions, particularly mitral stenosis. In the older individuals, 
particularly the senile cases, with intense athero- and arteriosclerosis and 
ulcerations of the aorta, a lesion proximal to the site of the embolism, may 
furnish one causative factor of the embolic process. 

The clinical history in cardiac cases is typical and striking. There may^be 
a fulminating course , terminating in death within a few hours or a few days 
(less than a week) after the onset, or a more protracted course in which case, 
the mortifying process in one or both lower extremities or even upper extremi¬ 
ties may have progressed so far that demarcation has set in, allowing amputa¬ 
tion to be done. Even here, the mortality is exceedingly high, death usually 
following within a short time after operation. 

1 Chodak, Royal Soc. Med., 1918-1919, Vol. XII (Sect. Dis. Children, p. 87). 

2 Stein, Surg., Gynec. and Obst., 1916, 23, p. 442. 



486 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


A typical course of a fulminating case is the following: With a distinct 
antecedent history of cardiac disease, the patient suddenly experiences pain 
in one or both lower extremities, or pain in the abdomen or back, followed 
by coldness of one foot or leg, loss of sensation, paresthesiae and loss of 
active motion. On examination the affected limb will be found to be blanched, 
soon after the onset, cold, flaccid, and somewhat tender above the zone of 
frigidity. The toes soon become livid, purplish or cyanotic, or the ischemic 
condition of the foot gives way to a mottling, patches of bluish purple appear¬ 
ing over the foot and lower part of the leg. The muscles of the calf of the 
leg, or the thigh frequently manifest fibrillary twitching. After 48 hours, 
this mottling gives way to a diffusely livid color, here and there scarlet patches 
shining through. The zone of coldness and of discoloration corresponds 
fairly well in extent, the upper portion of the discolored area showing exten¬ 
sive ecchymoses. Death may occur within 24 hours, or within a week, the 
patient becoming delirious, then stuporous, cardiac failure or cerebral 
emboli leading to sudden exitus. 

In protracted cases dry gangrene often develops; rapid evaporation takes 
place and the distal parts are the first to become mummified. A type of 
gangrene which in its objective manifestations can be compared to the desiccat¬ 
ing process seen in the drying parts in the dissecting room, is not uncommon. 
This form of gangrene, when it involves a considerable portion of the foot, 
or the whole foot, is almost always due to embolism. 

Where there is a more chronic course over a period of weeks or more than 
a month, the history may be as follows: With the story of an old cardiac 
complaint, there suddenly develop shortness of breath, precordial distress, 
possibly palpitation with or without vertigo and fainting. This is followed 
by pain in one or both lower extremities, loss of motion and loss of sensation. 
One or both limbs becomes rapidly cyanotic, the extent of the discoloration 
depending upon the situation of the thrombus. On physical examination, 
the dorsalis pedis, posterior tibial and popliteal arteries are regularly found 
pulseless. The femoral may or may not pulsate. Then the typical changes 
incident upon the development of dry gangrene ensue. The general condition 
of the patient will depend particularly upon the cardiac condition, and 
upon the presence or absence of infection. Usually there is more or less 
cyanosis due to the impaired cardiac action and evidences of a cardiac 
murmur. 

Such cases may last for a variable time (6 weeks or more) before amputa¬ 
tion is done. Although the operation of amputation through the thigh 
may be temporarily well borne, the mortality is exceedingly high. The 
patients may suddenly become stuporous. Evidences of cerebral embolus 
may appear, death occurring within a few hours or several days after 
amputation. 

Embolism at Bifurcation of Aorta.— The following cases taken from the 
author’s files, will illustrate the clinical and pathological findings. 

Case I.—Saddle embolism at bifurcation of aorta with complete occlusion 
of right, and partial of left iliac artery , gangrene of right lower extremity , ampu¬ 
tation , lethal outcome. 

A young woman (M. K.), 32 years of age, Mar. 28, 1912, reports that 5 years ago, soon 
after childbirth, she had had palpitation of the heart. She was free from symptoms until 
8 days ago when she fainted, had shortness of breath and precordial distress. On attempt¬ 
ing to leave her bed, she began to have burning pain in both feet and legs, and found that she 
could not stand. These symptoms were more marked on the right side. Both feet and 
legs, and to a lesser extent, the thighs, became blue and the patient lost all sensation up 
to the knee. The weakness in her right leg and foot became so marked that she could not 


EMBOLIC GANGRENE 


487 


raise her leg nor move the toes. The same symptoms developed to lesser degree in the left 
extremity. The right leg and foot have become more and more blue with marked tender¬ 
ness on pressure over the right popliteal space. The excitement attending her, leaving home, 
and the transportation caused palpitation, shortness of breath and cyanosis of face and limbs. 

Physical Examination. —The general condition was very poor, there being marked 
cyanosis, dyspnea, some exophthalmos, and dilated pupils. 

Heart. —Pulsation seen over mid-sternum; apex felt in 5th space, sounds of very poor 
quality; irregular action; occasional extra systole with compensating pause. First sound 
accompanied by systolic murmur, transmitted to left. Pulses equal, small, irregular, 
of low tension. 

Lower Extremities: Right. —Complete loss of muscular power, cyanotic with loss of 
surface warmth up to a hand’s breadth above the knee; big toe colorless. There are ecchy- 
motic patches of varying sizes up to 5 inches in diameter over the extremity. 

Left. —Cyanosis up to the ankle joint, and active motion in ankle joint absent. 

Vessels. —The femoral pulsation is absent on the right, present on the left. In the popli¬ 
teal, absent on the right, faint on the left. Both dorsalis pedes pulseless. The lower third 
of the right thigh hypersensitive, below which part there is complete anesthesia. Knee 
jerks absent. 

April 4.—This A. M. there is marked purplish discoloration up to the junction of the 
upper third with the lower two-thirds of the right thigh. In the left femoral and the popli¬ 
teal, there is a faint pulse. The left foot is cyanotic and edematous. The lips of the face 
are cyanotic, cardiac action being very irregular, a systolic murmur now heard. 

Liver palpable, general condition very poor. 

April 16.—Line of demarcation just below the right knee, the toes and leg mummified 
with loss of tactile sensation up to the knee. 

May 2.—Circular amputation of right thigh through the middle third well above the 
line of demarcation. Fat and muscle at the point of amputation looked gelatinous and 
glassy. 

May 5.—Patient is semi-stuporous, occasionally reacts and becomes very noisy, 
occasionally twitching of extremities, nystagmus, eyes deviating to left. Condition 
apparently due to cerebral embolus. 

May 6.—Patient became stuporous and ceased. 

Diagnosis: Chronic endocarditis (vegetations), embolism at the bifurcation of the aorta 
with partial occlusion of the left iliac; gangrene of right leg and impending gangrene of the 
left, and cerebral emboli. 

Pathologic Study of Arteries in Amputated Limb. —The popliteal and femoral arteries 
especially were sectioned and the complete dissection of the limb made. 

Extending from the junction of the upper and middle thirds of the leg and involving 
the rest of the extremity, there is dry gangrene. This area is sharply marked off from the 
healthy tissue by a definite line of demarcation. The vessels , arteries and veins, as traced in 
the healthy tissue show thrombi. The muscle tissues seem normal. The fat has a more or 
less gelatinous appearance. The femoral and popliteal arteries and veins are closed by 
thrombi. 

Microscopically, the walls of the femoral and popliteal arteries show a slight reactive 
inflammation, due to the beginning of organization of very small portions of the periphery 
of the clot. 

Conclusions. —The vascular lesions do not account for the occlusive thrombosis, and are 
slight and secondary so that the lesion responsible, for the peripheral thrombosis and 
gangrene must be sought above the point of amputation. 

The embolic involvement at the bifurcation of the aorta may be transitory 
or momentary as the symptoms would indicate, the clot becoming broken up 
into two parts each, suddenly and violently dislodged and thrown into the 
corresponding peripheral vessels, usually either the lower femoral or popliteal. 
When this is the case, we will expect to find both common femoral arteries 
pulsating (or absent but for a brief period) but both popliteal arteries pulse¬ 
less. Where there is a saddle shaped aortic thrombus at the bifurcation, 
all vessels of the lower extremities may be pulseless, or, if there be partial 
occlusion of one iliac, a faint or moderate pulse can be detected on the corre¬ 
sponding side. 

The history of transitory aortic emoblism with subsequent lodgment of 
fragments in the peripheral arteries of both lower extremities may be the 
following: Sudden onset of severe bearing-down pain in abdomen and lower 


488 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


back (oft likened to labor pains) with immediate coldness, pallor and weakness 
of both lower extremities and inability to use these limbs. Following this 
comes the advent of gangrene of both legs with absence of pulses in all the 
vessels from the popliteal downward, the femoral pulses being palpable. 

Case II.—Mitral stenosis , onset with symptoms of embolism at aortic 
bifurcation, subsequently only signs of bilateral embolic gangrene, autopsy 
revealing absence of clot either at aortic bifurcation or in the iliac arteries. 

E. R., age 48 reports that she has had signs of cardiac trouble for some 20 years 
(prior to Nov. 24, 1915). 

Patient has known that she has a cardiac condition for 20 years. She coughs after 
severe exertion, and has cardiac palpitation. During the past 2 weeks she has had severe 
attacks of cardiac palpitation necessitating her remaining in bed. She arose this morning 
(Nov. 24) at 6.30 and about one hour later she experienced severe pains in her lower lumbar 
spine and lower abdomen. The pains in the spine seem to have passed forwards. The 
abdominal pain resembled “labor pains” and continued for one half an hour. Then a 
sensation of coldness with the feeling of prickling spread over both legs, these becoming 
weak and then powerless. 

Physical Examination. —Marked cyanosis of lips with red flush of cheeks. A diffuse 
weak cardiac impulse is palpable, action is irregular and slightly accelerated. At the 
apex there is a presystolic murmur ending in a sharp short first sound. Pulses are equal and 
of fair volume, perpetually irregular. 

Lower Extremities. —A faint pulsation is felt in both femoral arteries, and no pulsation in 
both popliteal and dorsalis pedis arteries. The entire right lower extremity feels cold and 
the foot and leg are blanched. The left foot and leg are cold, the thigh is warm, color of toes 
is fair, nails are pink. Motion is normal in left lower extremity, whilst there is inability to 
move the toes and ankle joints of the right leg with preservation of motion in knee joint. 

Summary.—Embolism at bifurcation dislodged into both lower femorals or popliteals with 
more advanced occlusion of arteries of right than of left leg in a case of cardiac disease. 

Clinical Course. —After the initial pallor of the right foot, a puplish mottling set in, 
covering the foot and the distal half of the leg, over which region the parts were intensely 
coM to the touch. After 48 hours this color deepened, the foot and leg became 
livid and very cold to the touch. Here and there were peculiar scarlet red patches. The 
small veins of the skin separated the bluish and purplish mottling into irregular areas, and 
the uppermost portion of the discolored region was somewhat redder. The skin was the 
seat of diffuse hemorrhages, the bluish green veins being distinctly seen in the ecchymotic 
skin. . Portions of the ecchymotic skin then became dry, whilst others were moist. Above 
the skin at the middle of the leg the parts were slightly swollen and intensely tender. 

The left leg was also cold at first. Evidences of gangrene, however, did not set in until 24 
hours later, when the leg was cold up to the knee. The foot was then blanched, later mottled, 
the venous markings being even more distinct than normally, although not prominent, giving 
the leg the general appearance of a dissection specimen, the numerous veins and venules 
with their greenish blue blood standing out prominently against the white background, 
giving the whole surface the appearance of a geographic drawing. Here and there was a 
pale livid hue extending almost to the knee. Both femorals at this time were pulsating 
faintly, the popliteals, dorsalis pedes, posterior tibials pulses being absent. 

On Nov. 28 gangrene of both legs was well established: exitus on this day. 

Autopsy Findings— Mitral stenosis, dilated left auricle with antemortem clot in auricu¬ 
lar appendix; no embolism at bifurcation of aorta, nor in iliac arteries. 

Case III.-—An exquisite example of initial blockage of the aorta at the 
bifurcation with subsequent liberation of one iliac due to detachment of the clot, 
will be cited. 

M.M., female, 77 years, had been suffering with recurrent pains in the lower extremities 
for some four years When seen by the author (May 5, 1914) she had had a sudden 
attack of abdominal cramps and pain in both lower extremities with weakness and cold¬ 
ness of the legs nine days before. Some four days later, having been confined to bed 
S11 }ce the le & s showed considerable purplish discoloration, and had become quite 

cold and lifeless. According to her physician, pulsation in neither femoral artery could be 
detected. 

Examination on May 5, 1914. The right foot is gangrenous, dry, resembling a dried 
dissecting room specimen; the leg above and up to the mid-thigh is cold and bluish- the rieht 
femoral artery can be felt as a hard cord. ’ 6 


EMBOLIC GANGRENE 


489 


There is gangrene of the left leg in the early cyanotic and bluish stage up to the knee. 
There is good pulsation in the left femoral artery although none of the distal arteries can be 
felt. 

In view of the bilateral absence of the general pulses at the onset, and the 
subsequent establishment of good pulsation on the left side, the diagnosis of 
detachment and peripheral lodgment of clot was warranted. 

Diagnosis. —The recognition of embolic or thrombotic gangrene must be 
based upon the following facts: The existence of the proper etiologic factor 
(cardiac disease, aneurysm, etc.), the suddenness of the onset with the distri¬ 
bution of the gangrene, the affected territory corresponding to sudden oblitera¬ 
tion of one of the larger arterial trunks, popliteal, femoral, and iliacs. The 
differential diagnosis between embolism and thrombosis cannot always be 
made, for the gangrene may be due to extensive secondary thrombosis, rather 
than to the primary lodgment of an embolus in a larger vessel. The mere 
closure of an artery alone does not account altogether for the extent of the 
gangrenous process in many instances. Furthermore, the pathological 
examination of the amputated limb, too, may corroborate the view that 
secondary thrombosis is responsible for the extent of the lesion. Nor, is it 
always possible to locate exactly the site of the embolism or thrombosis. 
Although simultaneous involvement of both lower extremities with feeble pulse 
in the femorals speaks for saddle-shaped thrombus in the iliac, a similar pic¬ 
ture may be due to simultaneous lodgment of emboli in both popliteals with 
secondary thrombosis extending up to the femoral artery. The study of 
clinical cases, however, together with pathological findings have demonstrated 
that even where we strongly suspect saddle-shaped embolism at the bifurcation 
of the aorta, this portion of the vessel may be found free at autopsy. In 
such cases it may bevassumed with some justification, that the saddle-shaped 
embolus was broken up and dislodged, and thrown into both femorals or 
popliteals. 

When the femoral pulse is lost in both legs, the presence of a saddle- 
shaped thrombus is almost certain. When there are symptoms in both 
extremities, and the femoral pulse absent in one, present in the other, a saddle- 
shaped embolus may or may not be present. If it is, it occludes one iliac 
more thoroughly than the other. The femoral artery may be felt as a hard 
cord usually due to secondary thrombosis. The clinical picture may be 
complicated by sudden exacerbation in the limb which was at first but 
slightly affected, an argument in favor of the view that another embolus 
had been cast off in the corresponding vessel. Occasionally embolism or 
thrombosis of the external iliacs will give the symptoms of ischemia, which 
will be soon followed by improvement due to the establishment of collateral 
circulation through the internal iliac arteries. 


4 . Post-operative Embolic or Thrombotic Gangrene 

We are concerned here not with the pulmonary emboli and thrombosis, 
but merely with the lodgment of emboli in the peripheral arteries, where 
they may produce gangrene. Surgical operations seem to be a very com¬ 
mon cause, or at least seem to provoke, in some way or other, the detach¬ 
ment of emboli in the formation of thrombi in veins and in arteries. Schenk 1 
found that of the cases of thrombosis and embolism following operations, 58 
per cent occurred after the removal of large pelvic tumors. In 3204 myoma 

1 Schenk, New York Med. Jour., Sept. 6, 1902; also Am. Gynec. Soc., 1913. 


490 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


operations, 96 or 3 per cent were followed by thrombosis. McLean 1 in his 
studies of a series of 1310 laparotomies found 26 or about 1.9 per cent com¬ 
plicated by thrombosis or embolism. 

The production of gangrene of this type is not thoroughly understood. 
Doubtless traumatism to the iliac vessels or pressure on the popliteal in the 
Trendelenburg posture may explain some of the cases; or a complicating 
cardiac lesion may be the source of an embolus in others. There still remains 
a fairly large number in which no satisfactory interpretation of the patho¬ 
genesis has as yet been offered. 

Similarly in the cases of gangrene complicating pregnancy (so-called 
puerperal gangrene ), the causal factors have not been adequately clarified. 
Most of the reported cases have occurred after confinement, a very few during 
pregnancy and after abortion. 

5 . Thrombotic Gangrene in Healthy or but Slightly Diseased Vessels 

There is still another class of cases in which the etiology of the thrombus 
formation is not clear, and in which pathological studies have revealed a 
bland thrombosis of the peripheral vessels, in the territory of the dorsalis pedis 
and plantar arteries, that is undoubtedly the cause of the gangrene. It may 
occur in elderly individuals, who have slightly or moderately atherosclerotic 
vessels, or may occur in vessels that are practically normal save for plaques 
of thickened intima. These must be distinguished from the cases of thrombo¬ 
angiitis obliterans. The specific and characteristic lesions of the latter are 
absent, and the thrombotic process is less extensive, coming on suddenly, 
without the long history so characteristic in thrombo-angiitis obliterans. 
The author has been unable to find a description of this type of gangrene 
in the literature. 

Clinically there is the history of exposure to cold or other insult or trauma. 
Or, without a cause, one of the toes, usually the big toe, becomes cyanotic; 
the distal portion of the foot shows areas of blanching. The big toe, or the 
other toes, may show marked blanching on elevation, or the cyanosis may be 
so marked that blanching is masked. Sometimes pain is altogether absent, 
another distinguishing feature from thrombo-angiitis obliterans, as well as 
from the cases of acro-asphyxia. There may or may not be slight erythro- 
melia or reactionary erythromelia. Both lower extremities may be affected, 
although not simultaneously as in Raynaud’s disease. There may be a 
history of gangrene of one limb, presumably following a mechanical or 
thermal trauma. Or, no such history may be obtainable. Thus, the first 
symptom to be noticed may be the appearance of bluish or cyanotic spots 
or areas at the tips of one or more toes, usually the big toe or the big and 
adjoining toe. Rather significant, too, is the absence of pain in some of the 
cases. 

Low amputation may not suffice and re-amputation may have to be 
resorted to in some cases, at the knee or higher. 

Pathological studies have revealed that the larger vessels are practically 
negative, and the small peripheral arteries only are closed. Bland organizing 
thrombi are found in the territory of the dorsalis pedis and plantar vessels 
(Figs. 163 and 164). In such cases it is almost impossible to differentiate 
clinically between chronic acro-asphyxia to which thrombosis has been super- 
added, slight arteriosclerosis with thrombosis in the distal vessels, or delayed 
thrombosis following a so-called paralytic functional condition. The last 
1 Jour. Am. Med. Assn., Aug. 29, 1914. 


EMBOLIC GANGRENE 


491 


has been described by certain authors (Monckeberg) as responsible for those 
late cases of gangrene developing weeks and months after exposure to severe 
cold (angioparesis). 

From the diagnostic standpoint , the cases are interesting because they may 
be confounded not only with chronic acro-asphyxia, but with thrombo¬ 
angiitis obliterans and arteriosclerosis. The suddenness of the onset, the 
sudden disappearance of the pulses, and the rapid development of symptoms, 



Fig. 163.—Bland thrombosis in slightly diseased vessel. 


the absence of pain in some instances, the absence of evidences of marked 
arteriosclerosis in spite of the age of the patient, are rather characteristic; 
in thrombo-angiitis obliterans there is a long prodromal period in much more 
youthful individuals. 

Illustrative Case .—A survey of the clinical and pathological findings in a 
case observed by the author in 1914 will be instructive. 

In a man, L. S., 52 years of age (April 1, 1914), who had had none of the premonitory 
symptoms of arterial disease of the lower extremities, there was a history of exposure to cold 
with “frost bite” 7 weeks previously. Subsequently, though not immediately there¬ 
after, the big toe of the left foot became cyanotic, pain being absent. After some 6 weeks, 
during which gangrene slowly developed and spread from the big toe across the foot involv¬ 
ing all of the toes, amputation was deemed advisable. This was carried out just above the 
knee. The material for pathological studies thus afforded revealed the following: 

The specimen is in two parts, one portion consisting of the knee and upper third of the 
leg, the other of the remainder of the leg and foot. All the toes and about one inch of the 
foot above show the terminal stage of dry gangrene. A line of demarcation is well marked. 


492 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The branches leading to the internal saphenous vein are all free. The external saphenous 
vein is filled with postmortem clot. The popliteal vessels are not thrombosed. The wall 
of the artery is much thickened at the level of the head of the tibia. The anterior and 
posterior tibial vessels and the peroneal vessels are all free, and show no macroscopic lesion. 
The dorsalis pedis artery contains a fresh clot which is somewhat adherent to the vessel wall 
and is dark red in color. In the terminal portion of the dorsalis pedis artery, the clot has a 
light color and where the metatarsal branch and the digital branch of the vessel come pff 
from the main stem, the clot is lighter in color, and in the digital branch has a yellowish 
appearance and seems firmly united in the vessel wall. The digital branch referred to arises 



Fig. 164. —Organized bland thrombus in thrombotic gangrene, arteries being seat of 
moderate degree of arteriosclerosis. 

from the main trunk of the dorsalis pedis artery itself. Those branches for the other toes 
and the terminal portion of the metatarsal artery are all hidden in the gangrenous portion 
of the foot and toes. 

Microscopically the affected vessels showed none of the lesions of thrombo-angiitis 
obliterans, but the vessel walls were slightly atheromatous, enclosing the “bland type” 
of occlusive thrombus in various stages of typical organization. 

Clinical Course: —About the beginning of July, the big and second toes of the right foot 
became bluish, being unattended by pain. The cyanosis was followed by formication in 
this region, and the discoloration persisted for about a month when he was again examined 
by the author (August 3). 

Physical Examination. —August 3,1914.—The foot was very cold to the touch almost up to 
the ankle, the tips of all the toes being cyanotic. The sole as well as a portion of the dorsum 
showed distinct blanching without edema or tenderness. There was a slight increase of 
ischemia on elevation of the limb without eliciting any pain. A very moderate reactionary 
rubor was also demonstrable, and differed from that seen in thrombo-angiitis in that it 
appeared first only and above the ankle from which it extended gradually downward towards 
the toes. No chronic or constant rubor was present. 


EMBOLIC GANGRENE 493 

The dorsalis pedis and posterior tibial arteries were not palpable whilst the popliteal 
and femoral were found pulsating. 

The symptoms, objective manifestations and diagnostic methods of examination gave 
data strongly in favor of a repetition of a lesion identical with that of the other already 
amputated limb. 

The chronic cyanosis, the absence of chronic rubor and intermittent 
claudication, the short duration of the disease before the advent of gangrene, 
make a characteristic symptom-complex. Occurring in an individual 
beyond middle age with vessels already slightly atheromatous, the scope of 
diagnostic possibilities naturally is widened by virtue of the necessity for 
considering arteriosclerosis as a factor. 

From the pathological standpoint, the patent popliteal, peroneal, anterior 
tibial and posterior tibial arteries with bland thrombosis in various stages of 
organization in the peripheral arteries (plantar and dorsalis pedis) differen¬ 
tiate this type of case from thrombo-angiitis, and warrant its recognition as 
a separate entity until further researches will have been made. 

Theoretically, lesions of thrombo-angiitis but confined to small parts of the plantar 
arteries with superadded bland accretion thrombosis, would constitute a pathologic picture 
beyond the pale of even microscopic recognition. For, the detection of such minimal 
foci would require a complete study of every bit of the arterial course. 

6 . Embolism and Thrombosis Complicating Arteriosclerosis 

Embolism may occur when the larger arteries (particularly the aorta) 
are markedly diseased. Small thrombi attached to ulceration may become 
detached and lodged in the more peripheral parts of the circulatory system. 
In such cases, the symptoms are similar to those described as secondary to 
cardiac disease. This type may coincide with post-operative embolic gan¬ 
grene after operation on individuals with the arterial lesions referred to. 

Thrombosis of the peripheral vessels complicating arteriosclerosis has been 
described under the section on arteriosclerotic gangrene. The most character¬ 
istic cases are those in which the symptoms of threatening gangrene occur. 

7 . Embolism and Thrombosis in Acute Aortitis 

Inflammation of the aorta complicating gonorrheal infection is said (Guil- 
lain and Rendu 1 ) to have resulted in gangrene of the upper extremity from 
“obliteration” of the subclavian artery; and in gangrene of a lower extremity 
through embolism of the femoral artery. 

8 . Aortic Aneurysm and Embolism 

Gangrene of the leg and feet have been observed as a complication of 
aortic aneurysm, usually as a sequence of embolism. 

The Treatment of Embolic and Thrombotic Gangrene. —The modern 
approach in the therapy of embolic closure of the vessels of the extremities 
should be one of operative prophylaxis. By this we mean that every effort 
should be made to diagnosticate the initial blockage of the main or large 
artery of the affected limb, and to make accurate localization thereof, so 
that the thrombus or embolism can be removed in due time, the artery sutured, 
and the circulation restored. While this is not difficult either from the 
clinical or operative standpoint, in the case of embolic closure of the axillary 
or brachial artery, somewhat more acumen and experience are required for 
the timely and correct interpretation of symptoms due to similar occlusion 
of the femoral or popliteal artery. An awakened interest and a few germane 
hints may suffice, however, to stimulate the practitioner to the acceptance 
of this more advanced and fruitful attitude. 

1 Cit. by Roger and Gouget, Maladies des Arteres, 1915, p. 370. 


494 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The methods recommended for such diagnosis are discussed elsewhere. 

The following operative methods have been proposed for dealing with 
thrombosis and embolism of arteries: First, ligation; second, arteriovenous 
anastomosis; third, arteriotomy; fourth, arterial resection; fifth, arterial 
catheterization. 

1. Ligation has been suggested with a view to avoiding the dangers of 
embolism. However, Stewart 1 contends that when the diagnosis is certain, 
thrombosis is usually occlusive, the danger of embolism past; and there¬ 
fore does not recommend ligation. We are concerned here with the role of 
thrombosis and embolism in the production of gangrene, and certainly liga¬ 
tion can in no way improve the circulatory condition. 

2. Arteriovenous anastomosis at the present stage of our knowledge 
seems to be theoretical rather than practical. Stewart believes that in most 
of the cases reported favorable, even if the arterio-venous fistula remains 
patent, the blood deflected from the artery into the vein does no more than 
hinder the return of blood in those veins, producing a sort of passive hypere¬ 
mia. Stetten, 2 from his experimental studies, concludes that the operation 
is dangerous, and the results have been most unsatisfactory, except in a very 
small percentage of cases, and that even if the anastomosis functionates, which 
it rarely does, there is no possibility of circulatory improvement, and that the 
usefulness of the operation is restricted to an unappreciable minimum. 

3. Arteriotomy (embolectomy) is an operation which must be seriously 
considered if the diagnosis be made sufficiently early, and if operation be 
permitted before the effects of occlusion of the vessels have set in, namely, 
advanced gangrene. Success can only be obtained if the arterial wall is still 
undamaged at the site of the embolism, and before the secondary extensive 
thrombosis has occurred. The operation was first proposed by Sabanajew in 
1896. Stewart reported a successful case in May, 1907, in a man aged 61, in 
whom 36 hours after the onset of pain, the femoral was opened, and an embo¬ 
lus extracted and the artery sutured. Pulsation immediately appeared in the 
femoral below the point of suture, and also in the popliteal, but not in the 
tibial. Forty-two days later, the leg was amputated below the tubercle of the 
tibia, and evidences of good circulation were obtained at operation. 

Mosny and Dumont 3 were able to save a limb by the removal of an embolus 6 hours 
after its lodgment in the femoral artery. Murphy 4 removed a clot from the iliac and 
femoral in a case after gangrene had already set in, making an incision in the superficial 
femoral. By means of a spoon or scoop and catheter, the clot was dislodged, the catheter 
passed up into the aorta, a good flow of blood obtained and the artery sutured. He believes 
that in cases of aseptic embolism, immediate removal by division of the artery in the line of 
embolism or below should be resorted to. Although in his case he used a spoon and catheter 
for probing and dislodging the clot, he believes that aspiration through a catheter is a better 
means of removing the plug. If the catheter be divided on the slant, its open end can 
be easily introduced into the artery, and, unless the embolism is hard, it can be sucked or 
drawn into the catheter. He does not advise incision into the artery at the site of the 
embolism, because this region is already roughened, and the tendency to subsequent 
thrombosis is favored. 

Bauer 5 has reported a successful case of removal of embolism from the aorta just above 
the bifurcation through an incision into the artery made by the trans-peritoneal route. 
The embolus was about 3 cm. long, had the form of a molar tooth with two short roots, these 
lying in the iliac arteries. The symptoms referable to the lower extremities promptly 
disappeared, except for some pains in the left foot and calf. This operation, performed 3 
hours after the onset, was followed by recovery, the patient leaving his bed on the 25th day. 

1 Ann. Surg., 1915, p. 519. 

2 Surg., Gynec. and Obst., April, 1915, p. 381. 

3 Bull, de PAcad. de med., LXXV, No. 43. 

4 Jour. Am. Med. Assn., 1909, LII, p. 1661. 

6 Zentralbl. f. Chir., Dec. 20, 1913; also Zentralbl. f. d. ges. Chir. u. Grenzgeb., 1914, 4. 


EMBOLIC GANGRENE 


495 


The early removal of an occlusive clot from the larger arteries of the 
extremities—such as the brachial, femoral or popliteal—gives promise of 
being an effectual mode of coping with impending gangrene of embolic 
nature. Unfortunately, the practitioner is not aware of the value of imme¬ 
diate surgical intervention in such cases, and the re-establishment of the 
circulation is hoped for through the mere institution of conservative methods. 
The condition should be recognized at the very onset of the arterial block¬ 
age, and arteriotomy with removal of the clot should be advised. 

As soon as the following symptoms are in evidence, arteriotomy should 
be advised: pain in the affected extremity, coldness of the hand or foot, 
sensation of the parts falling asleep and formication, interference with 
motility, loss of sensation, increasing pallor and coldness with or without 
cyanosis; in short, the usual signs of abolishment of circulation. Coldness, 
pallor, and absence of pulses may be the only signs. 

A typical cardiac case with multiple detachment of emboli demonstrating 
the value of arteriotomy is the following. 

R. S., girl ii years of age was suddenly attacked with coldness, formication, and pain in 
the right leg and foot. The dorsalis pedis, posterior tibial and popliteal pulses became 
imperceptible, but gangrene did not set in because of the rapid development of the collateral 
circulation (May 25, 1923). 

June 8, 1923 it was noticed that the fingers of the right hand suddenly became cold. At 
8.30 A. M., when seen by the author, the hand and arm up to the upper fifth were found 
blanched and cold. The brachial, ulnar, and radial pulses were absent, but the axillary 
and beginning of the brachial artery were pulsating. 

At 10 A. M. arteriotomy under novocain anesthesia was performed. On exposure, 
after dissection of the axillary and upper brachial arteries, the former was found pulsating; 
the brachial found bluish, and distended with a clot. Careful liberation of these vessels 
from the surrounding tissues disclosed the fact that the clot extended to the origin of the 
superior profunda. The brachial and superior profunda were temporarily clamped with a 
serrefine, and a Crile compressor applied proximally to the pulsating axillary artery. On 
longitudinal incision into the anterior wall of the artery the clot, dark reddish in color, 
was spontaneously extruded. To ascertain whether no further minute clots were present, 
the axillary was allowed to bleed through the incision and then again controlled. Running 
suture completed the operation. 

The circulation in the hand and forearm was immediately restored but the radial pulse 
remained absent for a few hours, gradually returning to normal. Two weeks later the 
Radial pulse was still normal as well as the circulation of the hand. 

It is neither difficult from the diagnostic nor from the therapeutic stand¬ 
point to accomplish the localization of the embolus in the case of the upper 
extremities. Because of the accessibility of the brachial and axillary arteries 
to the touch and the deductions that perceptible or imperceptible radial 
and ulnar pulsations can afford us, the recognition of the site of the lesion is 
easy. 

In the case of the lower extremities exact localization may offer a some¬ 
what more intricate problem; but the extent of the coldness of the extremities, 
its upper limit, and the condition of the dorsalis pedis, posterior tibial, 
popliteal, femoral and external iliac pulsations may permit us to restrict 
the possible territory in which the clot may lie to within a very short distance. 

The following case is instructive even though the patency of the arterial 
channels beyond the site of the removed embolus could not be completely 
restored. 

In a young man operated upon for gangrenous appendicitis by a colleague 1 (Feb. 14, 
1920), the right forearm suddenly became cold, cyanotic and motionless early in the morn¬ 
ing of the third day after the operation. The brachial artery did not pulsate below its 
upper fifth. 


1 Dr. P. Aschner. 


496 


CIRCULATORY AFFECTIONS OF TIIE EXTREMITIES 


Feb. 17, some 3^ hours after the onset of symptoms, the author exposed the upper 
portion of the brachial artery at the site of the thrombus, under novocain anesthesia, and 
by arteriotomy removed the clot, about 2 cm. in length, closing the artery by suture 
according to Carrel technique. There was excellent pulsation in the brachial below the 
site of the clot and no leakage after completion of the suture. In spite of this demonstrable 
patency of the brachial artery below the site of the embolism and thrombosis, no pulsation 
could be detected in the radial artery. Tt was, therefore, believed that secondary clots 
had previously become detached and lodged in the peripheral vessels, or had grown upon 
the embolism (stagnation clots). 

Clinical Course. —Feb. 18, in spite of the reestablishment of the circulation in the lower 
brachial artery, the right hand was somewhat cold, but there was definite evidence of 
marked improvement- in its circulation. On Feb. 19, the color of the thumb looked doubtful, 
being somewhat cyanotic and cold. Furthermore, there were signs of muscular palsy and 
some tendency to contracture of the fingers in the flexed position. Extension of the hand 
seemed impossible, although motion of the fingers was excellent. 

On Feb. 20, after the application of dry heat in an electric baking apparatus in which 
a contact burn could have taken place, trophic disturbances became manifest over the 
posterior surface of the forearm. A long whitish area, suggesting dead skin, with loss of 
sensation over at least 3 inches X iH inches appeared. There was another similar smaller 
area over the posterior aspect of the wrist and the skin just above. Later in the day, the 
central portions of these areas showed blebs. 

Feb. 25, the fact that a certain amount of gangrene would develop was well established 
since the following lesions could be demonstrated: First— The trophic lesions. Second— 
Evidences of gangrene. Third— Circulatory disturbances. 

The trophic lesions: The areas of circulatory insufficiency were well demarcated on 
Feb. 25,there being an elongated area some 3 inches X i/^ inches surrounded by a well- 
defined narrow line of deep red, as if a red chalk mark had been drawn around it. Within 
this there was a distinctly white zone less than 1 cm. in diameter enclosing a central purplish 
space, in which the typical blebs of gangrene were to be seen. 

Evidences of gangrene: The thumb showed a deep purplish color; was somewhat 
withered, evidently in the early stage of a dry gangrene. 

Circulatory changes: Although the postero-external aspect of the forearm was fairly 
warm, the internal aspect changed color suggesting a possible future necrosis. Between the 
thumb and the dorsal trophic disturbance, over the thenar eminence and thereabout on the 
posterior surface, there was a peculiar ham colored red with diminished temperature due 
to marked circulatory disturbances. The four fingers, however, were in fairly good con¬ 
dition, of good color and the motility good. 

Feb. 23—6 days after thrombectomy—slight wrist drop developed, and there were 
definite sensory and motor phenomena, said by the neurologists to have been due to implica¬ 
tion of the ulnar and musculospiral nerves. In the region of the brachial wound there was 
some induration, possibly due to deep infection. 

March 8, chill and rise of temperature to 105.4 0 with a negative blood culture, the feve^ 
disappearing in 24 hours. March 12, again chill and temperature to 106°, and the blood 
culture showed hemolytic streptococci. March 16, some pus was evacuated from the 
brachial wound. An abscess of the right thenar space was evacuated on March 18, and 
on March 20, the temperature gradually attained the normal by lysis. 

April 7, the gangrenous area of the thumb had become well demarcated, and the 
terminal phalanx was disarticulated. A few days later the patient was discharged from 
the hospital. 

In May of the same year the condition of the hand and forearm was as follows: It was 
atrophic, weak, of a dusky red color, and the fingers purplish. There were trophic dis¬ 
turbances of the nails, which were discolored and poorly nourished. Hyperhidrosis was 
also present. In the dependent position, paresthesia and pain were very severe. Neuro¬ 
logic examination demonstrated marked impairment of the motor and sensory functions of 
the median and ulnar nerves. There were still small sequestra at the site of amputation, 
and these were spontaneously extruded in the course of the next 4 weeks. 

Postular exercises and electrical stimulation were given. Improvement rapidly took 
place, so that in a month the fingers could be semiflexed. Three months later a normal 
range of motion was reestablished, the atrophy of the muscles was almost abolished, and 
the color and texture of the skin approached the normal. 

It was reported that on Sept. 7 1 —7 months after the vascular occlusion—the radial pulse 
had returned (through collaterals?); one month later the patient was able to resume his 
work as a chauffeur. 


1 Personal communication from Dr. Aschner. 


EMBOLIC GANGRENE 


497 


Although successful from the purely technical standpoint, the radial 
pulsation was not restored until late, due to the presence of thrombi distal 
to the site of the embolism. Nevertheless, the operative procedure served a 
purpose in that an additional part of the brachial became patent, and the 
source of collaterals thereby widened. 

In view of the presence of a bacteremia, there obtained here an additional 
factor (probably toxic) predisposing to the extension of thrombi. It has 
been often observed by the author that stagnation thrombosis may spread 
rapidly from emboli in the larger arteries in cases of pneumonia and influenza, 
while the field of obturation is more apt to remain restricted and anastomotic 
paths conserved in pure cardiac disease and atherosclerosis. 

The question of removal of the embolus, therefore, should be entertained 
very early wherever an additional toxic element may vitiate the result. In 
the above case, although the first clinical manifestations of embolism were 
noted about 3^ hours before the operation, the occlusion was doubtless of at 
least 10 hours’ duration, judging from the appearance of the clot. This 
may be too late; for, on the one hand, time is given for the detachment of 
clot through the action of reflux currents and motion of the limb into more 
remote territories, and, on the other hand, rapid growth of the clot by 
stagnation, abnormal currents and vortices, and through the forces of ferment 
liberation, may be expected. 

That these factors need not be reckoned with to the same extent in afebrile 
and atoxic cases, and that the results are more favorable, the citation of an 
additional case will illustrate. 

It is a good example of successful removal of an embolus from the brachial 
artery and demonstrates that the removal of an embolus about 5 to 6 hours 
after its lodgment in the brachial artery may be followed by complete restora¬ 
tion of the circulation through the normal vascular paths. 

L. G., aged 57, was said to have chronic endocarditis with mitral murmur, there having 
been a previous history of a number of attacks of erysipelas. About September 14, 1922, 
he was suddenly seized with a cramp in the right leg, lost consciousness temporarily, but 
recovered without medical assistance. The right leg became cold, blanched, and gradually 
darker and darker, developing dry gangrene. 

The patient was seen by the author on September 20, at which time dry gangrene involv¬ 
ing the greater part of the foot, and moist gangrene over the upper part of the leg had 
already developed; the lower third of the thigh also being cold to the touch. None of the 
pulses from the femoral downwards was palpable. 

Diagnosis.—Embolic gangrene. 

September 21 (8:35 A. M.) a typical circular amputation (without tourniquet), was done 
by the author through the upper fourth of the right thigh, the femoral artery being found 
filled with recent clot. 

2.45 P. M. of the same day the nurse was unable to obtain a pulse in the right arm; she 
noticed that the fingers were very cold, the hand pale, and that the patient complained of 
numbness and weakness in the corresponding hand and forearm. This condition was also 
observed several hours later by physicians, who recognized the embolic nature of the arrest 
of circulation in the right upper extremity; but the matter was not reported to the author. 

The patient was seen by the author at 7.15 P. M. of the same day, and the following 
status noted: The general condition of the patient was fairly good; the hand and forearm 
were cold and pale; neither the right radial nor the ulnar pulsation was perceptible. On 
palpation along the course of the brachial and axillary arteries, the pulse was found absent 
below the lower margin of the teres major muscle. The diagnosis of embolism in the upper 
brachial artery was made, and the operation of arteriotomy was immediately advised. 

After consent was obtained, operation was performed at 9.06 P. M. of the same day. 

Operation. —The skin over the lower axillary and the upper part of the brachial artery 
was infiltrated with 1 per cent novocain solution, and about 2^ inches of the course of the 
brachial artery exposed in the typical fashion, and the point of obstruction located. At 
about the level of the origin of the superior profunda artery a clot could be distinctly felt in 
32 


498 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the artery, pulsation below this point being absent, and the arterial girth considerably less 
than that of the vessel above or at the site of the occlusion. 

A Crile artery compressor and one serrefine were applied above and below, and a small 
incision about K inch in length made longitudinally, immediately over the clot. Just as a 
compressing and milking movement was attempted in order to force the clot out of the 
opening, and as a portion of it protruded through the gap, the whole embolus was suddenly 
projected outward, evidently by virtue of a circulatory force within the artery itself. In 
spite of the presence of the clamps, bleeding was continuous, copious and non-pulsatile, so 
that more intensive compression both above and below was applied. As the slit was opened 
with two delicate forceps, the bleeding which continued in spite of change to the above 
measures, caused the sudden evacuation of a small shred-like clot, evidently a tail-piece or 
accretion clot, that had blocked either the superior profunda or was riding upon the embolus 
in the brachial. 

In view of the uncontrollable bleeding through the artificial orifice, it seemed evident 
that the artery had been opened just opposite to the point of origin of the superior profunda 
artery, through which a collateral reflux was going on. 

It was decided, in view of the importance of the superior profunda as an anastomotic 
channel, to attempt closure and suture of the artery without tying off this vessel. After 
thoroughly lubricating the vessel with sterile albolene, the longitudinal aperture was com¬ 
pressed and closed with the thumb and index finger of the left hand. Then arterial suture 
was begun from above downwards, with the finest silk (doubled) and the finest and smallest 
Kirby needles (Carrel pattern). Running suture was easily applied, the assistant pulling 
taut, tying the first knot, the last knot being tied by the operator. After the removal of 
the clamp not a drop of blood oozed out of the suture line, and it was not deemed wise to 
reinforce this. 

Pulsation and dilatation of the brachial artery below were immediately restored, and the 
pulsations were confirmed to exist in the corresponding radial and ulnar arteries by an 
assistant. 

Inspection of the fingers and hand immediately after the wound was closed demon¬ 
strated a return of color and warmth to the hand and forearm, and restored motility. The 
patient also noticed a prickling sensation throughout the fingers and hand. 

Although the incision in the arm healed by primary union and the pulses were restored 
and remained so, the patient succumbed subsequently to the lodgment of multiple emboli, 
one in the left external or common iliac artery, and another possibly in a vessel of the right 
half of the cerebrum. 

On September 28, 8 A. M., the left leg suddenly became cold and blanched, the femoral 
and the popliteal pulses being imperceptible. From then on the usual manifestations of 
early gangrene developed, the cyanotic discoloration of the foot and leg, and the coldness 
which extended up to the groin. 

Although the patient was seen about one hour after the lodgment of the embolus in the 
iliac artery and operation for it was advised, consent was withheld. 

September 29, the patient was distinctly weaker, pulse more irregular, and he was at 
times irrational. 

September 30, sudden left-sided palsy, cerebral disturbances, exitus. Up to the time 
of death, the right radial pulse remained as strong as the left and the circulation of both 
arms equally good. 

In short, a case in which embolectomy with removal of a large clot from 
the right brachial artery was successfully performed, with restoration of the 
circulation until death which occurred 9 days after the operation. 

Technique .—When the embolism is located in the brachial arteiy, the 
following technique will be found useful. 

Under novocain anesthesia and sharp dissection, the artery both at the 
site of the thrombus as well as for some 2 cm. above and below is exposed, 
kept moistened with saline and lubricated with liquid vaseline. The extent 
of the thrombus can then be easily determined both visually and by palpa¬ 
tion. After the application of a serrefine or arterial compressor above and 
below the clot, a site for arteriotomy is selected either at the very upper 
end of the clot or over it. A longitudinal incision is made either just above 
or over the clot with a spear pointed or triangular knife. The clot may 
be spontaneously extruded, if through collateral branches (or the superior 
profunda artery) the circulation in the segment within the compressing 


VASOMOTOR AND TROPHIC NEUROSES—GENERAL CONSIDERATIONS 499 


forceps is not completely arrested. If necessary, however, and to avoid 
injury of the intima, the thrombus is milked outward by digital compression 
above and below. Washing of the artery with saline and longitudinal suture 
of the artery in Carrel fashion completes the operation. 


CHAPTER LXXXVI 

THE VASOMOTOR AND TROPHIC NEUROSES—GENERAL 
CONSIDERATIONS 1 

Vasomotor and trophic phenomena may accompany a number of different 
diseases, such as other neuroses, or organic arterial and nerve affections. 
But there remains a large group of diseases divisible into distinctly differ¬ 
entiable clinical entities, some of which will be here described under the 
appellation vasomotor and trophic neuroses. A thorough comprehension of 
all of their manifestations is essential for a diganosis of the organic vascular 
morbid processes that they so closely imitate. 

The well-known clinical types include the following: (i) vasomotor; (2) 
sensory; (3) secretory; and (4) trophic disturbances. 

The vasomotor symptoms may be subdivided into local syncope, local 
asphyxia and local hyperemia. 

The sensory include paresthesia and pain, and in certain cases thermo¬ 
paresthesia and thermalgia are especially notable. 

Amongst the secretory we group anhidrosis and hyperhidrosis and anoma¬ 
lies of sudoriferous secretion. 

The trophic lesions are represented by gangrene or necrosis of lesser degree 
as well as atrophies, hypertrophies, and that unique type of nutritional 
phenomenon known as sclerodermal change. 

Distinctive Criteria. —There are sufficiently striking qualities that charac¬ 
terize these groups, and concern (1) the character of the pain, (2) the localiza¬ 
tion of symptoms, (3) the peculiarities of the clinical course, (4) the etiologic 
and predisposing factor, and finally, (5) the other signs of involvement of 
the sympathetic. 

1. The pain is never confined to the distribution of a single peripheral 
nerve or nerve root. 

2. The localization is signalized by a remarkable affinity for the peripheral 
distal parts, as fingers, toes, nose, ear, chin and tip of the tongue. . 

3. An intermittent chronic course which is not progressive. This feature 
is in striking contrast with the progressive course of organic vascular affec¬ 
tions such as thrombo-angiitis obliterans. 

4. The influence of previous infectious diseases, cold, or other functional 
neuroses and a neuropathic heredity. 

5. The coexistence of instability of the vegetative (autonomic and 
sympathetic) system, a sort of vasomotor lability, and often vagotonic 
phenomena. 

Not all of these maladies are complicated by gangrene and marked trophic 
disturbances. Those which can be mistaken for the organic vascular diseases 
will receive special consideration. 

1 For the latest views on capillary microscopy in these affections see Chaps. CVI, CVII, 
and CVIII. 



500 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The following will be discussed: 

(1) Atypical forms of vasomotor and trophoneuroses that are intermediary 
between the well known clinical entities. 

(2) Raynaud’s disease. 

(3) Erythromelalgia. 

(4) Acroparesthesia. 

(5) Chronic acroasphyxia. 

(6) Multiple neurotic gangrene. 

(7) Scleroderma. 

Although it is most useful, for purposes of clinical segregation, therapeutic 
indications and prognosis, to follow a grouping of the vasomotor neuroses in 
some such manner as Cassirer has indicated, we must keep in mind that, as 
yet, students and investigators of this subject are far from being unanimous; 
nor are they altogether in accord with the above categorical subdivisions of 
these disorders. Curschmann 1 will not even admit that erythromelalgia 
merits the distinction of being a discrete malady, and interprets the mani¬ 
festations as but a single “phase” in the course of vasomotor neuroses. 
Common to a number of these conditions, according to this author’s experi¬ 
mental work, is an abnormal type of vascular reaction or an absence of the 
normal arterial reaction in the affected extremities, when these are exposed 
to sudden temperature changes. 

Employing the plethysmograph, as applied by von Romberg and O. Muller, this author 
investigated the problem of estimating the arterial response to thermal influences, in 5 cases 
of Raynaud’s disease, 1 case of scleroderma, 3 typical instances of acroparesthesia with 
erythromelalgic phenomena, 2 cases of angioneurotic edema, and 2 patients with “inter¬ 
mittent claudication.” 

Muller’s researches on the vascular reaction in arteriosclerotic arteries led also to an 
amplification of our comprehension of what a normal response to cold and warmth should 
be. Subjecting the proximal portion of the healthy extremity—that which was not in the 
plethysmographic compartment—to cold, he recorded a sudden diminution in the volume of 
the distal parts. A similar result followed bodily pain. In arteriosclerotics, this reaction 
was less marked or absent, in consonance with the intensity of the lesion. Warmth would 
produce a contrary but slower and inconstant increase in volume. 

Adopting this procedure for investigation of the vasomotor neuroses, Curschmann 
approached this problem, as to whether a continuous or intermittent abnormal vascular 
tonus exists. 

In Raynaud’s disease and scleroderma, the normal reaction was absent. Warmth, at 
times, evoked a paradoxical arterial constriction. The conclusion was drawn that a primary 
disturbance of vascular innervation, therefore, must be a factor in this malady. So also, 
in his experiments in the acroparesthesia the normal experimental responses were missing. 

We refer the symptomatology in Raynaud’s and the allied maladies to the 
vasomotor system, and to disturbances in the whole vegetative apparatus, 
and perhaps correctly to the central portions of this system. Organic changes, 
however, have not as yet been discovered, and doubtless such are not present 
in the case of most of these affections. The free intervals and the intermittent 
course speak strongly against the existence of pathologic anatomic alterations, 
except in the case of chronic asphyxia and scleroderma. 

Some authors, stressing the close interdependence of the vegetative system 
and the internal secretions, would attribute the manifestations to endocrine 
dyscrasias. Others consider it more likely that a disorder of the vegetative 
system is responsible both for the derangement of the vasomotor innervation, 
as well as for abnormalities of internal secretions. 

As mere attendant symptoms (symptomatic form) the manifestations may 
accompany organic nerve and arterial disease, and hence the confusion and 
1 Curschmann, Miinchen. med. Wchnschr., 1907, No. 51, p. 2519. 


VASOMOTOR AND TROPHIC NEUROSES—GENERAL CONSIDERATIONS 501 

mistakes in diagnosis that are often made by experienced practitioners even 
up to this day. The recognition of the existence of coincidental organic nerve 
or arterial disease will do much towards classifying the manifestations as 
merely symptomatic , as opposed to the idiopathic or intrinsic complexes that 
we designate as vasomotor and trophic neuroses and subdivide in the forms 
indicated above. 

Theoretical Concept of the Neuroses of the Vegetative Nervous System. 

The clinical manifestations and their mode of origin have been variously 
interpreted by physiologists and clinical observers. Perhaps the most accep¬ 
table views are those according to which disturbances of the function of the 
vegetative centers are brought into causal relationship with the well-known 
clinical phenomena. It has been pointed out previously that the center in the 
corpus striatum may influence the centers in the midbrain in such a 
manner that the latter (with its subordinate parasympathetic and sympa¬ 
thetic centers) can maintain a certain threshold or state of equilibrium 
between the parasympathetic and sympathetic functions. Whilst Eppinger 
and Hess consider the so-called vagotonic complex as an expression of 
increased excitability of the parasympathetic paths and refer such alterations 
in irritability to an imbalance between the internal secretions—adrenalin— 
and an hypothetical “autonomin” (excitant of the parasympathetic), more 
recent observers would explain the variabilities in the responses of the 
vegetative system to changes in the higher nerve centers themselves. Dresel 
refers the para- and sympatheticotonic disposition or predisposition to 
functional alterations in the state of excitability of the corpus striatum , the 
latter, as previously stated, containing the regulatory mechanism. 

So that increased or diminished adrenalin secretion per se, and alone, 
could not be the cause of a sympatheticotonic or vagotonic disposition, as 
many authors believe. For an increased production of adrenalin should 
stimulate the midbrain regulatory mechanism in such a manner as to call 
forth an antagonistic response in other glands, with a view to restoring the 
old equilibrium. Therefore, it has been concluded that only disturbances in 
the central nervous mechanism can altogether explain the deficiency symp¬ 
toms. In short, a true central neurosis , or a functional dislocation of the 
excitability of the corpus striatum would be the more modern explanation 
of the clinical manifestations referred to derangements in the two large 
groups of the vegetative paths. 

When we attempt to explain the vascular neuroses, it is well to remember 
that these, just as the other vegetative neuroses (vagotonic and sympathetico¬ 
tonic), may be either of a chronic or paroxysmal type. In the former, would 
belong the cases of chronic vasomotor lability or instability; in the latter, 
those in which paroxysms or crises are in evidence, as in Raynaud’s disease. 

It is well known that there are evidences of functional disturbances of 
the vegetative system that appear suddenly in predisposed individuals, 
and then disappear. They may arise by reason of various causes. . Both 
psychic and reflex irritants may play a role; and pharmacologic excitation 
may modify the centers and the peripheral parts of the nervous system.. And 
so, in individuals with certain predispositions (e.g., parasympathetic dis¬ 
position) minimal excitement, psychic or sensory, may bring about an attack 
of asthma. In the healthy, such slight irritants may not evoke responses in 
excess of the physiological. In the vagotonic and sympatheticotonic 
dispositions, with central functional disturbances, paroxysmal symptoms 
may be brought about through irritants that attack the corresponding 
nervous system at any point, evoking manifestations in consonance with 


502 CIRCULATORY AFFECTIONS OF THE EXTREMITIES 

the existing hyperexcitability. Perhaps also in the special forms of vaso¬ 
motor neurosis the well-known crises or paroxysmal appearance of symptoms 
may be activated by irritants, the nature of which is unknown (toxic, reflex), 
on a predisposed central nervous system. 

Internal Secretions and the Vegetative Functions.—Many data seem to 
favor the view that internal glandular secretions (hormones) may not only 
act in a direct fashion, but indirectly through the nervous system. Thus, it 
was demonstrated that adrenalin exerts the same effect as when the sympathe¬ 
tic nervous system is stimulated. Clinically, too, nervous factors seem to be 
the exciting causes of many of the diseases of internal secretion, as well as 
being their most important manifestations. The close relationship, therefore, 
between the vegetative nervous system and internal secretions seems proven 
beyond peradventure. Not only does adrenalin selectively influence the 
sympathetic nervous system, but pilocarpin or physostigmin acts upon the 
nerve endings of the parasympathetic system in the same manner as electric 
irritation. 

Arterial hypotension has been regarded as a resultant of endocrine disease 
by a number of authorities since Addison first described epinephrin insuffi¬ 
ciency in 1855. A number of different blood pressure states also have been 
brought into relationship with abnormal activities of the endocrine glands. 
Numerous publications attest the general proclivity of modern authors to 
bring into causal relationship certain arterial diseases and those of the internal 
secretions that markedly affect the non-striated muscle of the vessels with 
consequent vasoconstriction. 

Antagonistic hormones, too, have been recognized as counteracting 
epinephrin in vasoconstricting effect. Thus the secretion of the thyroid 
is believed to neutralize or counterbalance the influence of epinephrin, so 
that certain authorities (such as Weber, Rolleston, and Williams 1 ) have 
suggested insufficiency of the thyroid secretion as a cause for the so-called 
senile, involuntary or decrescent type (Allbutt) of arteriosclerosis. Others 
take exception to this view. 

The importance of thyroid hormones in arterial affections receives further 
confirmation in the observation that arteriosclerosis is rather a common 
concomitant of cretinism. Wilson 2 regards the increased blood pressure 
frequently following the climacteric as due to the absence of the vasodilating 
influence of ovarian secretion. Engelbach 3 believes that the hypertension in 
these cases must be due to causes other than the disturbed secretion of the 
ovaries, or else it would occur in a larger percentage of cases. He offers 
clinical evidence in support of the theory that a certain selected group of 
cases of arterial hypertension is associated with endocrine dyscrasias. 

Krogh states that a hormone in the blood, probably derived from the 
activity of the pituitary gland, maintains the “normal” state of contractility 
of the capillaries. 

Mosenthin 4 expresses the view that in scleroderma we are dealing with 
deranged internal secretions with increased tonus of the sympathetic, basing 
his opinion on a study of the vegetative system in one of his cases, and on an 
analysis of the literature. What glands are responsible, however, he does 
not make clear. Cases are reported in which scleroderma is attended with 
disturbances in the thyroid, parathyroid, adrenal, sexual glands and hypo- 

1 Allbutt’s Diseases of the Arteries, 1915, I, 230. 

2 Wilson, S. A. K., Brit. Med. Jour., I, 1261. 

3 Engelbach, Wm, Jour. Am. Med. Assn., June 12, 1920, 74, p. 1619. 

4 Mosenthin, H., Arch. f. Dermat. u. Syph., 1913, Bd. 118, s. 613. 


VASOMOTOR AND TROPHIC NEUROSES—GENERAL CONSIDERATIONS 503 


physis. Of late years, there has been a distinct trend to associate thyroid 
disorders with scleroderma, though it is evident that the glandular malfunc¬ 
tion could be secondarily produced, reasoning by analogy, and recognizing 
that other glands, skin, bones and musculature suffer in this disease. That 
erroneous conclusions may be arrived at in attributing clinical complexes to 
certain endocrine disturbances, is illustrated by the case of Rasch, 1 who 
described a case of scleroderma supposedly influenced or caused by a hypo¬ 
physis lesion. At autopsy a normal hypophysis but with complete destruc¬ 
tion of one of the suprarenal glands was found. 

The role of the endocrine states in scleroderma is still a mooted question. 

Josefson 2 reports that certain cases of acrocyanosis were cured under 
thyroid therapy, believing the symptoms attributable to hypothyroidism. In 
a girl 13 years of age, he also saw improvement after organotherapy. The 
so-called acrocyanosis associated with tuberculosis is attributed by Rasch 3 to 
endocrine dyscrasia. 

Of recent years the pendulum has*swung towards the theory of endocrine 
influences in explanation of the vegetative functions. And perhaps too much 
importance has been attributed to lesions and derangements of the glands of 
internal secretion. Conversely, too little weight has been given the role of 
the vegetative nervous system per se, which in itself exerts a regulatory 
control of the activity of these very glands. 

As an example may be mentioned the influence relegated to the pancreas in the produc¬ 
tion of diabetes, and to the thyroid in evoking the Basedow complex. In reference to the 
former it may be said that Claude Bernard’s puncture was proof of the relation of the nerv¬ 
ous system and diabetes, and that the sugar metabolism is also influenced through the action 
of the nervous system upon the adrenal, liver, and muscle cells. 

So, too, in the case of essential hypertonia much importance has been attached to the 
adrenal gland. The role of the nervous system has been neglected. 

In diabetes Dresel and Lewy succeeded in showing important degenerative changes in 
the corpus striatum. Experimental work on rabbits developed that the exclusion of the cor¬ 
pus striatum was followed by a permanent hyperglycemia and glycosuria. From this the 
conclusion was warranted that at least in a percentage of cases of diabetes, localized changes 
in the brain stem are responsible. Just how these views can be harmonized with the more 
recent therapeutic results with insulin is a matter for conjecture. 

Dresel emphasizes the parallelism between essential hypertonia and the hyperglycemia 
of diabetes. In the one instance it is the blood sugar, in the other the blood pressure which 
suffers a rise in threshold. Because of these facts and the observation that even intensive 
alterations in the vessels themselves may produce no increase in blood pressure in the 
presence of properly attuned regulatory mechanism, have convinced this author that 
another explanation must be sought. He offers, therefore, the hypothesis that essential 
hypertonia is due to a derangement of the central regulatory mechanism, in the sense of an 
excessively high threshold for blood pressure; and that the arterial changes may be but 
secondary organic manifestations. 

In addition to these generalized expressions of central nerve derangements, 
more localized vasoconstrictor effects in circumscribed territories may be 
referable to central influences. When general, central, or peripheral (para¬ 
sympathetic or sympathetic) irritation exists, local attacks (of vagotonic 
and sympatheticotonic nature), such as asthma may result.. In the latter 
affection, psychic, sensory and toxic irritants may be the motivating factors. 
In the case of angiospastic forms of intermittent claudication a local hyper¬ 
tonic condition of the vessels of the lower extremities may be the response 
of a functional excitant. (For the theory of the reversal of the normal 
vasodilating reflex or response to a vasoconstrictor action, through altered 

1 Rasch, C., Dermatologen Kongress, Christiana, 1916. 

2 Josefson, A., Svenska la kare sallskapels handlungar, 1915, Bd. 41, p. 1. 

3 Rasch, Loc. cit. 


504 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


chemistry in the tissues in the obstructive arterial types of intermittent 
claudication, the reader is referred to Chap. XXVI.) 

Internal Secretions and Trophic Disturbances.— With the recent impetus 
given endocrinology, and the trend to explain numerous skin affections, 
scleroderma, Raynaud’s disease, and the other vasomotor and trophic 
neuroses on the basis of endocrine dyscrasias, opinions on the relationship 
of the internal secretions to skin lesions are worthy of mention. 

Thus Strandberg 1 in his summary concludes that: (i) the endocrine organs and their 
secretions have a distinct influence on the integument; (2) that endocrine disturbances can 
predispose to, and “produce” skin affections; (3) that some of the dermatoses whose patho¬ 
genesis is doubtful seem to have a common endogenous cause. Cases of family dermatoses 
show, not infrequently, a combination of various anomalies of cornification, hair develop¬ 
ment, nail growth, sclerodermal and vasomotor manifestations. 

The Hypersensitiveness of the Vegetative Nervous System. —Clinical observa¬ 
tions are being accumulated that point to the possibility of a condition 
of increased suspectibility or hyperirritability of the vegetative nervous 
system. It has been pointed out that climatic influences on the organism 
affect both the function of the endocrine glands, and the vegetative nervous 
system. Most of the deductions are pure hypotheses, but enough observa¬ 
tions are at hand to warrant entertaining some of these. In the case of 
tetany, the intimate relationship between the endocrine functions and the 
nervous system seems to have been proven beyond peradventure. 

I. n . c . e rt a i n animals, it has been shown that the autonomic nervous system varies in its 
sensibilities with the seasons. In rabbits irritation of the heat center by acupuncture has 
proven the varying and seasonal susceptibility of this center. Further data that concern 
the vacillating irritability of the vegetative nervous system are derived from the clinical 
observations, that so-called eczema death 2 and disturbances of the heat center occur in a 
seasonal way. In the former, a hyperexcitability seems to occur in the spring time, while 
in the latter, crises or periodic variations in the susceptibility of the vegetative nervous 
system would seem to take place. 

The unusual and interesting disease known as “idiopathic cutaneous 
atrophy, Erythromelie, ” has been regarded by some as due to endocrine dys¬ 
crasias. A short description of this malady will be found in the chapter on 
Scleroderma (Chap. C). 


CHAPTER LXXXVII 

THE SKIN AND THE VEGETATIVE NERVOUS SYSTEM 

So important is the control of many of the functions of the skin by the 
vegetative nervous system, that a general discussion of its influence, and a 
summary of the nerve paths and of the vasomotor manifestations in the 
skin may afford an apt explanatory prelude to the clinical description of the 
vasomotor and trophic affections. 

1 Strandberg, J., Beitr. z. Frage d. Bedeutung d. inneren Sekretion. 

2 Eczema death is mentioned here as a manifestation of the varying susceptibility of the 
vegetative nervous system, for it is believed that the cases of sudden, inexplicable death 
occurring in infants suffering from so-called constitutional eczema, may be due to status 
lymphaticus, or sudden cardiac paralysis occasioned by vagus malfunction. 



THE SKIN AND THE VEGETATIVE NERVOUS SYSTEM 


505 


The integument in its vascular and other component parts, including the 
hair follicles, the sweat glands, and the pigment cells, is under the control 
of the vegetative nervous system. The contractile elements of the skin, 
the vessels, the hair follicles, and the smooth muscle are affected through 
direct stimuli , namely, by substances that course in the blood and in the tissue 
fluids; or, indirectly through the nervous system. Centers lying in the spinal 
cord, and governing these functions are in their turn modified and influenced 
through the quality and warmth of the blood, through psychic impulses, 
or impulses emanating from the periphery. In this way, vegetative skin 
reflexes are brought about. 

One of the most commonly observed examples of the vegetating functions 
is the reaction to heat and cold. Whenever, by virtue of external cold, the 
temperature of the body would tend to drop, a regulatory function is set 
into action. The vessels of the skin contract, and the blood cannot find 
its way into the superficial layers of the skin; thus, radiation of heat is pre¬ 
vented. Conversely, with the body overheated, dilatation of the skin vessels 
takes place, and increased radiation. If this function is inadequate, the 
action of the sweat glands is brought into play. 

In this mechanism, two separate forces or impulses are set into activity: 
firstly, a direct action upon the vessels and muscles of the hair follicles which 
contract through cold (reacting contrarily to heat); and secondly, a reflex 
is set into motion, whose impulses pass through the sensory skin nerves to 
the vegetative centers in the cord, and thence centrifugally, bringing about 
contraction or relaxation of the muscular elements of the skin and increased 
perspiration. 

The Vegetative Reflexes in the Skin. —These include the responses that 
take place exclusively through the route formed by the nerve paths and 
nerve centers. Two groups have been recognized. In the first group the result 
of irritation is limited to a territory that closely approximates the region 
of stimulation. The reflex arc is probably confined here to the spinal cord 
without participation of the higher centers. As examples may be mentioned 
the contraction of the smooth muscle of the nipple areola; and the so-called 
reflex dermatographia. 

Whenever larger areas react, we speak of reflexes of higher order (second 
group). We may mention, to illustrate, the remote action of vasoconstrictor 
types after cold foot baths, and also the pilomotor reaction that may extend 
so as to involve a whole extremity or part of the body. 

Whenever the reflex becomes still more extensive so as to implicate a 
large part or the whole of the body surface with chilly sensations and goose 
flesh, the higher centers (cerebral) are probably at work. Whereas such 
extensive responses usually require rather severe and intensive irritants, in 
certain conditions susceptibility may be so heightened that very slight 
excitation suffices. It has, therefore, been assumed by a number of authors 
that generalized reflexes are dependent upon certain internal conditions. 
Given a certain threshold of excitability of the corresponding centers and 
possibly a certain predisposition of the peripheral vegetative organs, we have 
the possibilities for reaction to but limited or minimal external influences. 
With a certain degree of receptivity that is tantamount to a full nerve load, 
very slight impulses may lead to a discharge; and this explosion, as it were, 
follows certain existing nerve paths. Secondarily thereto, changes in the 
innervation of the vegetative organs of the skin may follow. 

Alterations in the vegetative innervation of the skin of psychic course 
(blushing, goose flesh) may expose emotional states no longer under control 
of the will. 


506 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Certain general concepts regarding the lability of the vegetative nerve 
innervation must be kept clearly in mind for a comprehension of the diseases, 
such as Raynaud’s and erythromelalgia. The skin reactions are subordinate 
to so many conditions, that we are often unable to draw conclusions regard¬ 
ing the condition of the vegetative nervous system, or, indeed, of the nervous 
system in general. What may be regarded as a morbid reaction both as 
regards intensity and feebleness in one case, may still be within the physio¬ 
logical in another case. Many of the conditions that determine the reaction 
may vary at different times in the same individual; others may be con¬ 
genital, hereditary or acquired. Of the various coefficients, the following 
may be mentioned; the condition of the skin, the nervous status, the momen¬ 
tary psychic state, chemical influences (metabolism, internal secretions, auto¬ 
intoxication), and so forth. 

The Nerve Paths .—The fibers for vasoconstriction controlling the hair 
follicle muscles over the whole body surface are traceable to the dorsal and 
three upper lumbar roots, the sympathetic centers lying at corresponding levels 
in the spinal cord. 

The cervical sympathetic contains the preganglionic vasoconstrictor, 
pilomotor and secretory sweat paths for the face. The vasodilator and sweat 
inhibiting paths for the face emanate from the cranial autonomic system; for 
the trunk and the extremities, fibers emanate also from the dorsal and upper 
lumbar segments that leave the spinal cord through the posterior and not 
through the anterior roots. In the peripheral sensory nerves of the skin 
there are fibers for all the constituent functions of the vegetative skin 
innervation. 

It is believed that sensory paths and centers exist for the various skin 
functions (vasoconstriction and dilatation, pilo-erection and blood secretion), 
for, these activities are independent. 

The vegetative skin reflexes take place through the following reflex arc— 
the sensory paths constitute the afferent limb of the arc, being traceable from 
the skin through the skin nerves into the spinal ganglion and posterior root 
into the spinal cord, then communicating with the vegetative center of the 
lateral horns. For the vasoconstrictor, pilomotor, and secretory fibers the 
efferent limb passes through the anterior root, the ramus communicans albus, 
and the sympathetic ganglion through the spinal nerve. The self-inhibiting 
and vasodilator fibers pass through the posterior nerve to the peripheral 
nerve. For vegetative skin reflexes of the higher order the interpolation of 
the center in the mid-brain may be assumed. 

The Vasomotor Phenomena of the Skin 1 .— Although the mechanism of 
all the varied pictures presented by or due to active constriction or dilatation 
of the smaller vessels of the integument is not altogether understood, it may 
be well to briefly discuss the nature of some of these for a better comprehension 
of the clinical affections. In the chapter on Capillary Circulation we have 
alluded to the response on the part of arterioles, capillaries and venules, 
both to direct influences, as well as to nerve stimuli. The total capillary loop 
may be affected through the nervous system even by emotion, or externally 
through cold or other impulse (even mechanical as in dermatographia), 
active constriction of the loop may result. Thus, narrowing or dilatation of 
the vascular loops may occur. The greatest fluctuations are noticed in the 
arterial limbs. Some authors believe that there is a special innervation for the 
arterial limb in view of the clinical manifestations. 

The skin presents either a normal color or deviations therefrom: These 
are increased redness, transitory rubor, chronic rubor, induced rubor or 
1 For data to be gained from Capillary Microscopy, see Chaps. CVI et seq. 


THE SKIN AND THE VEGETATIVE NERVOUS SYSTEM 


507 


reactive hyperemia, reddish blue cyanosis or asphyxia, complete pallor 
(syncope), and the so-called marmorated appearance. 

The blood content accounts to a great degree for the normal color of the 
skin, and under ordinary circumstances only a part of the capillary territory 
is filled. The arterial blood tends to flow rather through the deeper and 
shorter communicating paths into the venules. When there is hyperemia, 
rubor or redness, we assume an increased filling of the superficial vascular 
strata with red arterial blood, with adequate patency of both afferent and 
efferent channels. At the same time the blood stream is more rapid than 
normal, and the skin feels warm under such conditions. 

The various forms of rubor, transitory rubor of neurogenic origin, or 
permanent rubor following chronic obstructive arterial disease, and reactive 
hyperemia (induced or reactionary rubor, or erythromelia) are described in 
detail elsewhere. Here we need merely mention that a reactive hyperemia 
may take place in a normal individual after a temporary impediment to the 
circulation has been withdrawn. And so it is visible as a reactive ischemia 
due to the application of an Esmarch or Martin bandage, after Bier’s method 
of producing stasis, and after cold or pressure anemias. Opinions vary as to 
the explanation of this phenomenon, some believing that an exhaustive or 
paralytic state in the capillaries occurs, others, that there is an active dila¬ 
tation of the cutaneous vessels. Bier had already suggested the theory that 
by virtue of metabolic derangement, and absence of oxygen, an active 
dilatation of the capillaries ensued. This theory is somewhat in accord 
with the recent views of Hooker who had demonstrated that metabo¬ 
lites or tissue products are capable of inducing an active dilatation of the 
capillaries. 

On the other hand, reflex vasoconstriction in the arterioles and smaller 
vessels has been laterally interpreted (Zak) as a neurogenic response to 
accumulating waste products (COO, and more properly lactic acid in the 
muscles; and is assumed to occur in territories poorly supplied with blood 
after exertion. 

Reflex action may also account for the capillary response, as is seen after 
irritants, such as cold. A livid or cyanotic discoloration of the skin presup¬ 
poses dilated vessels and stasis. In view of the arrest or sluggishness of the 
circulation, the temperature of the part also becomes lower, and the skin 
may become cold to the touch. Neurogenic spasm in the smallest arteries 
with stagnation in the capillaries and venules (as in Raynaud’s disease) 
may cause asphyxia, or, a combination of circulatory weakness (in obstructed 
arteries) and the effects of gravity (as in the pendent position), may bring 
about the same color. Not infrequently can the chronic dilatation of the 
venules and their immediate channels of higher order be demonstrated in a 
condition of chronic dilatation, when the cyanotic or livid toes in thrombo¬ 
angiitis obliterans are depleted of their blood by elevating the extremities. 
Then we note that ischemia sets in because the capillaries cannot be.filled 
in this position, and that the venous paths, either by virtue of dilatation of 
the venules or vasoconstriction of the larger veins, fail to empty themselves, 
and remain as livid markings. 

Active contraction (vasoconstriction) of the vessels of both skin layers 
produces complete pallor or syncope. 

A reticular patchy lividity or reddish and purplish discoloration of the 
skin produces the so-called marmorated appearance. We distinguish the 
livid and the hyperemic form of cutis marmorata. The former occurs 
usually after exposure to cold. It is not known to what extent a reflex 


508 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


nervous mechanism, or in how far direct action of thermic influences are 
responsible. 

It is often impossible to segregate the effects of purely vegetative nerve 
function from the other forces liberated, or already existent in the various 
morbid entities affecting the vascular system of the extremities. In inter¬ 
preting the vasomotor manifestations of the organic obstructive diseases, we 
have to take into account (i) the hydrostatic, mechanical and gravity factors; 
(2) the central and peripheral reflexes; (3) the reflexes evoked through changes 
in local circulation (ischemia on elevation); and (4) the local influence of 
metabolites on the capillary and venule territories. 

1. The first of these is discussed in detail in the chapters on Obstructive 
Arterial Affections. We need merely admonish the clinician, here, that 
whenever organic interference with vascular patency impedes the flow and 
diminishes the force of the stream, the state of fulness of the peripheral 
capillaries and venules is influenced thereby. Indeed, changing position of 
the limb may alter the circulatory conditions so as to give manifestations 
of incongruous nature, easily mistaken for those of nerve origin. They may 
be summed up as being of the nature of rubor , cyanosis or asphyxia , ischemia 
or syncope , or simultaneous combinations of any of these. 

2. The reflexes capable of calling forth alterations of the state of con¬ 
tractility in the vessels of the integument are also referred to elsewhere. 
For clarity, we may note here that even emotional states and the nervous 
habitus are not without influence through the higher centers; and peripheral 
afferent impulses such as cold, motion and trauma are clinically known to 
produce striking effects. 

3. If a limb in which the circulation is impaired through arterial obtura¬ 
tion be raised, depletion of the distal surface vessels is produced, and thereby 
localized ischemia or anemia. 1 Per contra in the hanging position of the 
limb a condition of rubor, cyanosis or intense cyanosis alone may develop. 
To what extent are these appearances of purely hydrostatic origin; how far 
are vasomotor influences at work; and what are the direct effects of local 
tissue changes or products responsible for the responses in the arterioles, 
capillaries and venules? These are questions that cannot be categorically 
answered, but the mere placing of the queries should arouse food for thought, 
and a correct attitude of interpretative analysis. 

Let us analyze but one phase, that of artificially induced ischemia on 
elevation of such a limb. What are the forces besides the hydrostatic, the 
gravity, the impaired force of the stream that are then brought into play, 
and that could modify or cause reaction in the peripheral vascular territory? 

4. As a result of the depletion, automatic constriction of the arterioles 
and venules could be predicted in conformance with known laws. But, is 
there not a simultaneous elaboration of metabolites in such an ischemic terri¬ 
tory that would make for dilatation of these paths? 2 Clinical observation 
recognizes that dilatation of the capillaries and even of the venules does 
actually occur. Have the vessels already dilated in the elevated position, 
and is the pallor merely due to mechanical forces and inadequate circulatory 
power? Or, does vasodilatation begin only when the limb begins to hang 
down, and does it require the filling of the vessels to evoke the intensified 
response? 

To answer these questions studies on the morphology of capillaries, and 
on the capillary pressure in the toes held in such positions, should be made. 

1 See application of these terms by extension, in Chap. X on Local Circulation. 

2 See work of Krogh, Dale and Hooker, Chap. VII. 


DIAGNOSIS AND LOCALIZATION OF VEGETATIVE NERVE LESIONS 509 


And only then will we know which of the forces, mechanical, neurotic or 
chemical, plays a dominant role. 

The Cutaneous Responses to Thermic and Actinic Irritants .—It has been 
observed that rays of long wave length develop warmth energy and act as 
heat irritants, whilst rays of short wave length, when absorbed, bring about 
chemical changes. The action of sun rays is well known, the primary hypere¬ 
mia, the consequent painful reddening, swelling and sunburn. Protracted 
exposure to light may cause a permanent dilatation of the capillaries. 

A moderate degree of heat brings about dilatation of the capillaries of 
the skin by direct action upon the contractile substance of the capillary 
endothelium and the musculature of the smallest vessels. It has been shown 
that the limbs or the neck of an experimental animal when deprived of 
nerve continuity still respond by a hyperemic reaction to hot air. Very 
intense heat causes an effect similar to that of cold in the constriction of the 
cutaneous vessels, particularly in the small arteries. Later, however, with 
continued exposure a hyperemia of the congestive variety, similar to that 
produced by cold, is noticed. In this the arteries are constricted, the capil¬ 
laries and veins dilated. 

When severe cold is of but short duration, arteries and capillaries are 
contracted, and when the external temperature rises again a hyperemic 
reaction occurs. Continued cold produces a paralysis of the vasoconstrictor 
action with a livid hyperemia, in which the venous portion of the capillary 
loop is engorged. In the case of cold, however, reflex action is more apt to 
take place as is borne out by the observations that a distant part of the body 
may respond synchronously. As an example, we may quote the contraction 
of the cutaneous vessels of the other limb when one is plunged into cold water. 
The immediate effect of cold comprises the action of both a reflex and direct 
mechanism. So, too, does this obtain in the case of heat (Rehberg and 
Krogh). 


CHAPTER LXXXVIII 

DIAGNOSIS AND LOCALIZATION OF VEGETATIVE NERVE 

LESIONS 

The multiplicity of vasomotor centers makes possible the substitution of 
subordinate centers to compensate for lesions that bring about vasomotor 
disturbances. This can be all the more effectively brought about, in that the 
minor centers have a greater independence of action than the superior. On 
the other hand, this far-seeing provision of Nature has its draw-backs. For 
the recognition of the seat of lesions of the vasomotor system is consequently 
made difficult, and oft impossible. The existence of two systems of contrary 
powers and their susceptibility to varied reflexes from all over the body 
still further complicates diagnostic work. One may conclude, therefore, 
that it is quite impossible to make deductions regarding the pathogenesis of 
vasomotor disturbances from their character and distribution. Perhaps 
only where the vasomotor derangements are closely limited to the course and 
distribution of certain peripheral nerves, can we diagnosticate the seat of 
the lesion. 



510 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Deficiency symptoms in the vasomotor system show great tendency to 
recovery, a fact that is easily explained by the substituting action of numerous 
other centers. On the other hand, however, when we are dealing with the 
results of irritation of such centers or paths, other centers cannot act as 
surrogates, and no compensatory action takes place. With continued irri¬ 
tation we do not expect any abatement of clinical manifestations until the 
excitability of the corresponding nerve segment ceases and is followed by 
paralysis. For an understanding of the clinical cases of vasomotor disturb¬ 
ance, we must remember that through reflex paths irritation of the vaso- 
motors can persist for a long time. So, too, it is observed that irritation 
within the vasomotor system has a more potent action than the paralytic 
causes. Therefore, whenever we see vasomotor symptoms of long duration, 
we should look to reflex irritation as possible causes rather than to paralytic 
conditions. 

Although no final knowledge regarding the localization of lesions in this 
domain is at hand, some of the salient facts that clinical observations and 
pathological conditions have furnished may be worthy of recapitulation. 

Cerebral Lesions and Localization. —Vegetative disturbances following 
lesions of the cerebrum with motor and sensory symptoms regularly occur on 
the contralateral side. This would indicate that vegetative fibers, as well 
as motor and sensory fibers undergo complete crossing on their way to the 
periphery. 

It is well known that in those cases of Brown-Sequard palsy, where the 
lesions reside in the cervical cord, the vasomotor paralyses take place on the 
side of the lesion. And so it is assumed (Depisch) that the crossing of the 
vegetative paths occurs somewhere between the thalamus and the cervical 
cord. 

Vasomotor disturbances on the opposite side are reported as resulting from operations 
on the brain (Schlesinger 1 ). Nothnagel also describes such derangements complicating 
cerebral lesions. 

_ Rossolino 2 reports a case with attacks of Jacksonian epilepsy attended with edema and a 
livid discoloration of the affected upper and lower extremities. The temperature of the 
hand was_ 2-3 0 C. lower and the temperature on this side of the body was also i° lower. 
At operation a cyst was found in the anterior frontal gyrus of the opposite side, and after 
evacuation of the cyst the motor power of the extremity, which had been diminished, and 
the circulatory phenomena returned to normal. 

In a study of the vasomotor disturbances in hemiplegia, Goldstein and Parhon 3 found in 
13 out of 18 cases diminished temperature on the paralyzed side; in 4 no differences. 

Mager 4 describes a bluish discoloration of the skin below the middle of the paralyzed leg 
with lowering of the skin temperature in a case of right-sided hemiparesis. Autopsy showed 
a small apple sized-tumor involving the lower part of the central convolutions. 

Deficiency symptoms in cases of disease of the cerebrum, where large 
ganglia are implicated but not wholly destroyed, are associated with distur¬ 
bances in the vegetative processes of the contralateral side in the form of 
paralytic or irritative phenomena. 

Amongst the paralytic symptoms may be mentioned palsies of the 
ocular sympathetic and palsy of the vasomotors; of the irritative symptoms, 
occasionally mydriasis, increased constriction of the cutaneous vessels, in¬ 
creased secretion of sweat, the salivary glands, and mucous membrane. 

The vegetative paths crossing in the medulla oblongata for the eye, the 
vasomotor and sweat glands of the face are believed on the other hand to 

1 Schlesinger, Arch. f. Dermat. u. Syph., Festschrft. Kaposi, 1900. 

2 Rossolino, Deutsch. Ztschr. f. Nervenh., 1895, 6, p. 76. 

3 Goldstein and Parhon, La Roumaine med., Apr., 1899. 

4 Mager, Vide Obersteiner, Arbeit, a. d. neurol. Inst., 1907, XVI. 


DIAGNOSIS AND LOCALIZATION OF VEGETATIVE NERVE LESIONS 511 


connect directly with the same side of the body. The crossing point of these 
fibers, therefore (Breuer and Marburg 1 ), would have to take place between 
the pons and the internal capsule. 

The Vasomotor Paths for the Trunk and Extremities .—The cases of apoplec¬ 
tiform bulbar paralysis would seem to indicate that the crossing point of these 
fibers lies somewhat lower than that of the vegetative paths for the face. 



Fig. 165.—Decussation of vegetative nerve paths. (After Depisch) 

P = pyramidal paths K = vegetative paths for the head 

St + E = vegetative path for the trunk and extremities 

For, the clinical cases demonstrate that the vasomotor lesions occur on the 
contralateral side (Fig. 165). 

For elucidation of diagnostic interpretations the following recent views 
concerning the cerebrospinal vegetative paths may be of some value. They 

1 Breuer and Marburg, Quoted by Depisch. Wien. Archiv. f. inn. Med., 1920, 1 , p. 191. 




















512 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


may serve as an aid to localization when additional data will have been 
forthcoming. 

1. The vegetative paths from the cerebrum and the large ganglia of the 
brain-stem undergo a crossing on their way to the periphery. 

2. The decussation is complete at a level of the lowermost portion of 
the cervical cord; and below this the fibers undergo no further crossing. 

3. The decussation of the paths of the ocular sympathetic and of the 
vasomotor and secretory (sweat) impulses is accomplished in the region of 
the pons. 

4. The crossing point of the vasomotor and secretory paths for the trunk 
and extremities would appear to take place somewhere in the neighborhood 
of the pyramidal decussation. 

In short, these vegetative paths cross lower than those of the head, 
though higher than the motor fibers. 

These facts are in consonance with the clinical observation that either 
crossed or homolateral disturbances of the vegetative function can occur in 
lesions of the superior cerebrospinal tract. 

There would, therefore, be a region in which lesions would implicate 
vegetative paths before any decussation takes place and with homolateral 
derangements as a sequence. 

Pharmacologic Tests of the Vegetative Functions. —The three poisons, 
adrenalin, pilocarpin and atropin, are mainly used. Of these adrenalin 
acts on the whole sympathetic system; pilocarpin only on part of the para¬ 
sympathetic. The latter may be regarded as a substitute for that hypo¬ 
thetical substance—autonomin—which, according to Eppinger and Hess, 
normally keeps the parasympathetic nerve endings in a constant state of 
excitability. 

Adrenalin is a poison that acts as an excitant on the points of junction 
between the sympathetic nerve endings and the end organs (myoneural 
junctions). Tests for the production of general or local symptoms have been 
evolved, with a view to estimating the irritability of the sympathetic system. 

Injection of adrenalin (1 cc. of 1 :1000) subcutaneously causes normally 
the following reaction: after a few minutes palpitation, feeling of distress 
and tremor of the extremities, and local pallor and blanching of the face ensue. 
In individuals whose sympathetic system is hyper excitable, the reaction is 
excessive; the whole body may shake, there being precordial distress, cardiac 
pain, perspiration and even transitory collapse. 

Persons whose parasympathetic system is over excitable suffer little or 
no reaction after adrenalin injection. However, by reason of the inordinate 
vagus response, these individuals show numerous extra systoles. 

A reaction of excessive glycosuria is also regarded as a sign of hyper- 
sensitiveness of the sympathetic; absence of such, a vagus susceptibility. 

Responses on the part of the blood pressure, too, have been interpreted 
as of value in this connection. A rapid reaction with an abnormally high 
adrenalin blood pressure curve is said to be characteristic for a hypersensitive 
sympathetic system. 

Loewi believes that mydriasis following the instillation of 1-3 drops of a 
1 :1000 adrenalin solution in the conjunctival sac indicates defective tonus 
of the vagus or hypersensitiveness of the sympathetic. 

Pilocarpin, since it excites the parasympathetic system, is employed to 
estimate the responsiveness of the latter. The reaction after subcutaneous 
injection of 1 cc. of a 1 per cent solution is observed. The normal effect 
is a feeling of heat, perspiration, redness of the face and increased salivary 


VASOMOTOR AND TROPHIC DISTURBANCES 


513 


secretion. When the reaction is excessive, it indicates an increase of the 
irritability of the parasympathetic system, or generalized hypersensitiveness 
of the whole vegetative nervous system. 

A tropin has been used to detect the influence of the vagus on arhythmia. 

If symptoms supposedly due to over excitability of the vagus disappear 
after atropin injection, then confirmation of their vagus or parasympathetic 
nerve origin is at hand. 


CHAPTER LXXXIX 

VASOMOTOR AND TROPHIC DISTURBANCES IN LESIONS OF 
THE CENTRAL NERVOUS SYSTEM 

Intensive emotions may in susceptible individuals be followed by the 
appearance of pruritus or urticarial types of eruption. It is well known that 
severe shocks or psychic insults may cause the hair to turn grey, and a partial 
or total alopecia may result. Paroxysmal or long continued swelling of the 
skin may occur upon the paralyzed side after cerebral injuries—expressions 
of vasomotor disturbances—and even ungual dystrophies and anomalies of 
hair growth may complicate. Almost all the forms of trophic disturbances 
may be associated with spinal cord diseases. 

In myelitis we occasionally find bullous eruptions and herpes zoster. 
During paroxysms of tabetic origin, crises of herpetic eruption or urticaria 
or purpura have been observed. 

Herpes zoster is regarded as a reflection of disease of the spinal ganglia; 
an expression of abnormal increased excitability of the peripheral sensory 
neuron, or more probably of the peripheral vasosensory motor neuron. It 
may also attend lesions of the sympathetic gangliated cord. 

Tabes Dorsalis. —Trophic disorders here will hardly be confounded with 
the vasomotor and trophoneuroses, except in the case of associated malum 
perforans. Spontaneous gangrene has also been reported as complicating 
this disease. As a rule muscular atrophy involving large muscle groups, 
trophic affections of the joints and bones, and the so-called tabetic arthro¬ 
pathies are the well-known evidences of trophic derangement. 

Syringomyelia and Gliosis Spinalis. —The manifestations of disturbed 
nutrition are exceedingly varied, very often in the form of small vesicles or 
larger blebs over the hands. After rupture of the blebs, indolent ulcers 
develop. Wounds and cicatrices so often encountered over the hands of these 
cases are usually due to an inability to perceive pain and thermic impulses, 
and hence burns readily occur without the knowledge of the patient. Remak, 
Schlesinger and Oppenheim describe reddish blue discoloration of the hand 
and forearm (vasomotor phenomena). More extensive trophic disorders 
may take the form of bone necrosis, destruction of the terminal portions of 
the digits; or, if infection supervenes, phlegmonous processes may be expected. 

A peculiar appearance of the hands with enlargement simulating that of 
acromegaly has been observed (Schlesinger, Oppenheim). Even a myxoe- 
dematous change in the skin may be associated. Marinesco is responsible 
for the term “main succulent” as descriptive of a striking alteration in the 
consistency and texture of the soft parts of the hands. A diffuse swelling 
especially of the dorsal aspect sufficient to mask the underlying bony and other 

33 


514 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


landmarks, often attended with vasomotor phenomena, is regarded as 
characteristic. By virtue of muscular atrophy, a narrowing of the hand 
may take place. Arthropathies are frequently associated. 

A consideration of these manifestations will facilitate differentiation from 
the other forms of vasomotor and trophic neusosis (Chap. XCIX ). 

Injuries of the Spinal Cord. —The relationship between the nature of the 
vasomotor disturbances and the character and extent of the spinal cord lesions 
has not been definitely established. After total transverse lesions extensive 
vasomotor palsy of regions below the level of injury are often seen. They 
may, however, occur after incomplete interruption in continuity of the cord, 
and may be present in spastic conditions. Even so-called “vasomotor 
disturbance of the lymph system” has been described by Marburg and 
Ranzi, reflected in the condition of pasty swelling of the leg, following spinal 
cord lesions. With the vasomotor disturbances there may be trophic dis¬ 
orders, decubitus, vesicle formation and ulcers. 

These authors describe the following picture: The legs are swollen, the skin tense and 
stretched, glistening, of a waxy white color, occasionally bluish, the skin devoid of the usual 
characteristics of edema; or occasionally, too, edema, cyanosis, and coldness of varying 
degrees are observed. 

Vascular dilatation may appear over the paralyzed region; later coldness 
and cyanosis, signifying chronic vascular relaxation. Vasomotor disturb¬ 
ances are also responsible for the engorgement of the corpora cavernosa in 
such cases. 

In Brown-Sequard’s symptom-complex (unilateral transverse lesion) the 
skin may be reddened and warmer on the same side; later on, this may give 
way to a chronic condition of coldness and cyanosis. An interruption of 
the vasoconstrictor fibers of the lateral column of the same side is given as 
the explanation therefor. 

Decubitus may occur rapidly after traumatic lesions of the spinal cord. 
Kroh saw it develop 18 hours after injury; Henneberg on the morning follow¬ 
ing the trauma; and Krause emphasizes the unfavorable significance of its 
rapid advent. Decubitus may occur in places that are not subject to pressure. 
Total transverse lesions of the cord are not necessary for the development of 
such lesions. 

Two factors deserve recognition as of etiologic importance in the neuro¬ 
genic type of decubitus; namely, alterations in the circulatory function of the 
affected parts, and the direct influence of pressure, which, in most instances 
at least, is a factor. Nevertheless, the occurrence of acute decubitus with 
central nerve lesions has been so frequently described by competent observers, 
that a mechanical, traumatic or pressure effect has been proven to be not 
essential. 


CHAPTER XC 

NEUROTROPHIC DISORDERS IN SPINA BIFIDA 

Syringomyelia and spina bifida occulta may be complicated by trophic 
lesions that should not be confounded with those due to impaired circulation. 
Those associated with spina bifida occulta may occasion doubts as to diag¬ 
nosis. These, however, should be easily dispelled if we remember that in 
the latter, the arterial pulsations are normal, that sensory derangements of 


NEUROTROPHIC DISORDERS IN SPINA BIFIDA 


515 


the lower lumbar and sacral nerve roots or segments are usually present, 
and that true gangrene is absent. 

We are interested here merely with those vasomotor and trophic mani¬ 
festations that may lead to difficulties in differential diagnosis. A short 
resume of the salient features of the affection, however, may clarify 
doubtful points. 

Spina bifida occulta is said (Recklinghausen) to be attributable to an intrauterine healed 
myelomeningocele. According to this theory there should be a defect in the dura, but this 
is not always present. Hair growth and tumors are frequently found at the site of the 
defect in the spinal column. This manifestation is explained by the fact that in intrauterine 
life tissue elements are displaced. According to other authors (Marchand) cystic dilatation 
with spina bifida exists in intrauterine life with healing and spina bifida occulta as the end 
product. The existence of mixed tumors, fibromyomata, myofibromyomata is explained 
on the assumption that an intrauterine myelomeningocele, the product of the healing 
process in spina bifida occulta arises; and that through the traction of the scar, the skin, 
musculature and connective tissue become transferred or displaced into the depth and even 
into the spinal canal; from such, elements of neoplasms may arise. 


Symptoms of Spina Bifida Occulta. —These may be divided into: (i) 
those at the site of the sacral cleft; (2) those resulting by reason of involve¬ 
ment or lesions of the spinal canal contents, namely, the cauda equina, and 
the nerve roots and peripheral nerves. 

We are concerned only in this connection with the sensory, vasomotor 
and trophic disturbances. The latter will receive detailed consideration, 
whereas the other symptoms will be given merely passing mention. 

1. The Local Symptoms .—Of these the abnormal hypertrichosis is the 
most important, being noticeable in the region of the cleft. Cicatricial 
changes in the skin, with elephantiasis deformation, dimples, telangiectases, 
localized hyperhidrosis, funnel-like retraction of the skin or pseudo fistula 
formation, or abnormal depressions on this region—all these should arouse 
the suspicions of spina bifida occulta. But in many cases a sacral deficiency 
may exist even under normal skin. 

Occasionally a small tumor may be felt under the skin, which in itself is 
suggestive of spina bifida occulta. Any tumefaction in this region should 
arouse suspicion of the existence either of a spina bifida vera, or cystica, 
or one of the occult or concealed variety without protrusion of the contents 
of the spinal column. A tense elastic consistency would point to the former, 
a lobulated more solid nature to a lipoma over an occult variety. Local 
subjective symptoms include, vague pain, particularly on changing the 
position of the body or on exertion, probably due to traction of the cauda 
equina or nerve roots. 

2. Nerve Lesions of the Cord or Cauda Equina .—From the diagnostic 
standpoint it is valuable to know (Muller) that sensory irritative symptoms 
are absent when the lower part of the spinal cord is diseased, but paralytic 
symptoms are present, the latter in part as disassociated sensory phenomena. 
When alteration occurs in the cauda equina from compression due to a tumor 
or from traction, sensory, irritative manifestations are intense, and paralytic 
symptoms for all sensory qualities appear simultaneously. 

From the therapeutic and operative standpoint, it is important to deter¬ 
mine whether the cauda equina is mostly involved. For in the latter case, 
more is to be expected from therapy. Indeed, the cauda is capable of under¬ 
going some regeneration after operative work. Muller believes that when 
the trophic centers for the motor fibers in the spinal cord and the trophic 
centers for the sensory fibers in the spinal ganglia are conserved, regenera- 


516 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


tion of axis cylinders and medullated sheaths may occur after the deleterious 
forces in spina bifida have been put into abeyance. 

Disturbances Due to Lesions of the Nerve Apparatus. —These comprise 
neuralgia, pain in the region of the cleft, irritative or paralytic symptoms 
in the perineal region, genito-urinary apparatus and the lower extremities. 
It may not be necessary to give a detailed account of these here, since they 
are well know^n, resulting from congenital degenerative processes. Club¬ 
foot, pes cavus, trophic disorders of the lower extremities, particularly of 
the feet, and bladder symptoms, particularly enuresis, are amongst the most 
common manifestations. 



Fig. 166.—Trophic ulcer in the plantar aspect of clubfoot in a case of 
spina bifida. (Beck) 


Vasomotor and Trophic Disturbances. —Sensory disturbances of varying 
intensity, not always confined to the territory of certain nerves, usually 
coexist with other deficiency symptoms. There may be either irritative or 
paralytic symptoms. Sensibility may be either diminished, or tactile anes¬ 
thesia, especially for pain and temperature, may occur. Usually the hypes- 
thesia or anesthesia is limited to the foot or a part of the foot, or to a small 
territory oyer the leg or thigh. The various sensory disturbances may not 
be equal, inasmuch as tactile sensation may be conserved coincidentally 
with diminution or absence of temperature and pain sense. Or, the usual 
symptoms of cauda equina lesions may be present, with the typical saddle 
shaped area of anesthesia, sometimes attended with paroxysmal pain. 
Diminished pain and temperature sensation is rather characteristic for spina 


NEUROTROPHIC DISORDERS IN SPINA BIFIDA 


517 


bifida occulta. In the mild cases sensory disturbances may be slight or 
absent. Irritative phenomena and neuralgias indicate participation of 
the cauda. 

As for the vasomotor and trophic derangements , these are usually limited 
to one lower extremity comprising bluish red discoloration of one or both 
lower extremities or parts of the extremities, involving the foot or leg, and 
atrophy of an extremity with poor development of muscles of the whole leg. 

Mai perforant is considered one of the characteristic manifestations (Fig. 
166). Complicating this condition osteomyelitis, sequestra, necrotic bone 
particles, loss of toes, with consequent deformity of the foot and phlegmonous 
processes, have all been described. Amputation is required in a number of 
cases, after which healing may be poor. Secondary ulcers may necessitate 
reamputation. Ulcers may appear even in more central parts. 

Motor disturbances not infrequently accompany the above, with slight 
paresis or weakness of the single muscles, and even extensive paralytic 
complexes; more rarely irritative motor phenomena, such as fibrillary 
twitchings and spasms. 

An instructive case reported by Brickner 1 is worthy of brief citation, for the type of 
trophic lesion is well exemplified. 

S. H., female aged 18, presented herself for examination December, 1907, because of an 
extensive ulceration of the inner and flexor aspects of the great toe of the left foot, indolent 
in appearance and with foul discharge. 

She was a native of Jenkoping, Sweden, where at the age of 7 the second left toe was 
ulcerated from what was presumed to be frost-bite. This ulceration recurred each winter, 
and at the age of 12, partial amputation of the toe was required. 

Three years later (aged 15) the stump of the toe ulcerated and the phalanges necrosed. 
Six months later the fifth toe ulcerated, refused to heal, and was amputated. The first 
phalanx was necrotic. The wound was laid open and this bone was removed. Slowly 
the wound healed, without granulating , after the head of the first metatarsal spontaneously 
discharged. Specific medication seemed to exercise no influence. The dorsalis pedis, 
popliteal and posterior tibial vessels pulsated normally. 

In April, 1908, the two remaining toes (third and fourth) ulcerated and the two last 
phalanges of these were removed, leaving stumps. The foot was then quite edematous, 
but not painful, although there developed at this time a plantar ulcer near the base of the 
third toe. 

Over the lower lumbar and upper sacral regions, extending down from the third lumbar 
vertebra is a circular tumor about 4 yi inches in diameter, symmetrically situated over the 
midline. This tumor was present since birth and has grown with the patient. In the 
spine no cleft can be felt. Tests show sensory paralyses of the left lower extremity. 
Roentgenogram shows a cleft in the left lamina of the fourth lumbar arch. The fifth lumbar 
arch is not of normal shape. 

Clinical diagnosis: Spina bifida occulta associated with congenital lipoma over the lower 
end of the spine; cleft in the fourth lumbar arch with a lesion involving the posterior fourth 
and fifth lumbar, and first, second and third sacral roots or cord segments. 

Operation, July 3, 1908: The sac was removed, the nerve roots were reduced into the 
spinal canal, and the dura was sutured over them. The lumbar aponeurosis was closed over 
the hiatus by a plastic operation. 

The ulceration in the third toe had progressed and the plantar ulcer had also increased 
in size, exposing the head of the second metatarsal bone. 

By September 28, these ulcers were healed without any bone necrosis, and the patient 
was again discharged with a raised sole on her right shoe and crutches. In November the 
plantar ulcer reopened. During the next few months the ulcers improved and relapsed, and 
others developed. The patient was readmitted to the hospital. 

July 26.; Typical Pirogoff amputation. All the blood vessels appeared quite normal. 
Primary union. 

Pathological report (amputated foot): The vessels were practically normal, but there 
was marked bone atrophy. This atrophy was found in portions of the bone remote from 
the inflammatory process. The nerves of the foot showed no degenerative changes. In 
the immediate vicinity of the ulcers there were moderate inflammatory changes in the 
nerves. 

1 Brickner, Am. Jour. Med. Sc., April, 1918, p. 473. 


518 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XCI 

VASOMOTOR AND TROPHIC DISORDERS IN PERIPHERAL 

NERVE LESIONS 

Some of the symptoms, particularly the trophic disorders associated with 
peripheral nerve lesions may simulate manifestations attending organic 
obstruction of the arteries. 

The characteristic changes of the integument after nerve lesions are not 
altogether the sequence of altered circulatory conditions. The effects of 
exclusion of trophic nerve influences have already been given consideration. 
Regarding the circulatory derangements some authors describe these as 
anemia and venous hyperemia. In the former the skin may be pale, dry, and 
brittle; in the latter, tense, glistening, bluish red or almost cyanotic. These 
alterations do not seem to depend upon the seat of the nerve injury, but 
rather are related to fortuitous mechanical factors. Inactivity and atrophy 
of the musculature play a role in influencing the influx of blood. Perhaps 
the impaired venous return due to deficient muscular action is also an impor¬ 
tant factor; indeed, this mechanism seems to suffer more than the arterial 
influx. Although the bearing of direct trophic nerve influences upon the 
nutritive condition of the peripheral tissues is an important one, many 
commentators emphasize the preponderating influence of altered or defective 
circulation as a cause of the trophic lesions. 1 

Breslauer, in experimental work on the circulation in extremities whose main nerves had 
been injured, comes to the following conclusions: That after interruption in continuity 
of large peripheral nerves or posterior roots the local powers of reaction of the vessels may 
remain undisturbed in the anesthetic territory for a short period (about i week). Subse¬ 
quently, however, the vascular responses are partly lost. Whilst active vasoconstriction 
may be conserved, active vasodilatation upon peripheral nerve irritation becomes lost. 
Superficial anesthesia of the skin and the mucous membrane js associated with diminished 
vasodilating responses due to inflammatory and other irritants, whilst the vasoconstricting 
power remains unimpaired. 

According to these findings the absence of normal reactive hyperemia 
would be of great significance as a factor in the causation of trophic disturb¬ 
ances. 2 The normal integument must adjust itself constantly to the exigen¬ 
cies of external conditions and respond to numerous deleterious influences. 
As long* as the normal physiological vascular reaction is present, active local 
hyperemia can readily set in, and healing may take place. This means of 
defense is lost when the vessels in a tissue no longer respond; infection is 
inadequately combatted, and degeneration of tissues ensues. 

The rubor and erythromelia of thrombo-angiitis obliterans and arterio¬ 
sclerosis may be interpreted as one of Nature’s modes of supplementing or 
counterbalancing local circulatory deficiencies. 

After peripheral nerve injury, particularly those injuries due to bullet 
wounds, two types of manifestations may develop and mimic the symptoms 
of arterial disease. In the first there are the effects of complete loss of 
continuity of the peripheral nerves; and in the second irritative phenomena 
due to partial nerve injury. 

1 Breslauer, Deutsch. Ztschr. f. Chir., 150, p. 51. 

2 The important role of direct nerve influences on the nutritive integrity of the tissues is 
described elsewhere. 


VASOMOTOR AND TROPHIC DISORDERS 


519 


1. Symptoms with Complete Nerve Destruction.— Anesthesia, cyanosis, 
and pallor may occur and are due to the exclusion of the fibers inhibiting 
the vascular mechanism. These fibers cross or travel in the peripheral nerves. 
In addition there may be absence of the excretion of sweat, wrinkling of the 
skin, hyperkeratosis, loss of hair and stunted growth of the nails. The 
cyanosis and pallor may give a confusing clinical picture. The anesthesia 
and trophic disturbances, however, may speak strongly in favor of nerve 
lesions. 

Sciatic Nerve Injury .—When trophic ulcers develop after injury to the 
sciatic nerve, they do not usually appear until several months have elapsed. 
Besides the nerve trauma, repeated mechanical excitation of the affected 
peripheral part is required (rubbing and pressure). Hence the same localiza¬ 
tion of the ulcerations is observable as in mal perforant. Without trans¬ 
verse section of the nerve, the peripheral lesions do not usually follow. The 
ulcers have little or no tendency to heal spontaneously; they are rebellious 
to local treatment and persist for months or years without improvement, 
being complicated from time to time by attacks of local infection. Amputa¬ 
tion may eventually become indicated. 

Leriche 1 claims that perifemoral sympathectomy (decortication of the 
artery) in its course through the upper part of Hunter’s canal may bring 
about healing; and that an equally good result may follow resection of a 
neuroma of the proximal end of the cut sciatic nerve, if such be a complica¬ 
tion. Indeed, this'author attributes the trophic ulcers of this type to the 
reflexes engendered in such neuromata. Only temporary healing of the 
ulcers may follow removal of the neuroma, whilst permanent cures have 
been observed when nerve resection and repair are done. 

2. Irritative Phenomena Attending Partial Nerve Lesions. —The symp¬ 
tom of pain so often noted with the irritative nerve lesions is one that may 
cause confusion with the intense pain of thrombo-angiitis obliterans. Other 
associated symptoms, however, would permit of the differential diagnosis. 

Neuralgia with or without vasomotor accompanying symptoms is 
frequently observed after bullet wounds implicating the larger nerves of the 
extremities. 

The pain that follows injuries to both sensory and mixed nerves may be 
intense if the median nerve and the tibial nerve are involved (Mauss-Kriiger 2 ). 
It may be of great severity and obstinacy with hyperesthesiae and paraesthe- 
siae; and usually attended with somewhat less marked vasomotor and trophic 
disorders. Rubor and swelling are coincidental phenomena, and roughly 
correspond to the territory of the pain and the paraesthesiae. The distal 
parts of the extremities are sites of predilection. The balls of the toes are 
usually affected in the injuries of the tibial nerve, and also the terminal 
phalanges of the first three fingers in median nerve lesions. The hyper¬ 
sensitiveness of these parts makes even the slightest tactile impressions 
unbearable, and renders function impossible. 

As the result of the traumatic lesions of nerves, extensive cicatricial 
strangulation and penetration with connective tissue result, with some 
endoneural involvement, so that a partial disorganization of the nerve on 
cross section can be demonstrated. Sometimes the nerve is completely 
torn, and after cicatrization, although in apparent organic continuity, may 
be regarded as having suffered complete interruption of functional impulses. 

1 Leriche, Lyon Chirurg., 18, 1921, p. 33. 

2 Mauss-Kriiger, Bruns’ Beitr. z. klin. Chir., 1917, 108, p. 163. 


520 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The fact that some cases are attended with severe pain, that others with 
similar lesions do not suffer at all, would arouse the suspicion that causes 
outside of the cicatricial tissue are responsible. Some authors suggest that 
there is a general neurotic predisposition, a sort of neurotic component that 
has to be reckoned with. Given a preformed nervous potentiality, an 
accentuation of the sensory threshold is brought about through the injury. 
This suffices, in predisposed individuals, to keep these in a condition of con¬ 
stant hyperexcitability. In this latter state centrifugal impulses that ordi¬ 
narily do not cause irradiation into sensory territories are intensive enough 
to arouse the sensation of pain. 

Vasomotor and Trophic Symptoms. —Some authors describe the skin 
as moist, edematous, livid, thinned out and as easily injured. The transverse 
furrows are obliterated, the integument reddened, parchment like and shiny. 
Trophic ulcers are to be expected whenever slight traumata, such as burning 
with cigarrettes, pressure of tight shoes or other insults, unwittingly take 
place. Hypertrichiasis is a striking and important symptom. The nails 
grow abnormally fast, become friable and distorted, and show transverse 
ridges. Hyperhidrosis occurs because of the irritation of the sympathetic 
fibers. Since the secretion of sweat is dependent upon sympathetic and 
not upon vascular influences, we accept this phenomenon as a symptom 
characteristic of nerve lesions. It occurs when the nerve lesion is incomplete. 

In the descriptions elsewhere given, sensations of cold are mentioned, as 
also edema, marked cyanosis, blotchy skin and differences in temperature. 
Even mat perforant has been observed. A severe degree of trophic disturb¬ 
ance is usually only present in those cases where considerable interruption 
in the nerve paths has occurred. Marked trophic disturbances of the foot 
and leg may attend lesions of the sciatic nerve. Both the intense pain and 
the neurotrophic manifestations may disappear after successful nerve 
suture. 

Vasomotor Trophic Symptoms Following Bullet Wounds. —Our knowl¬ 
edge of these manifestations has been considerably broadened and clarified by 
observations made during the Great War on results of bullet wounds involv¬ 
ing the pheripheral nerves. In a discussion of vasomotor and trophic dis¬ 
orders, the secretory and sensory must also be mentioned, since these may 
play a part in the symptom-complex. A brief summary of recent obser¬ 
vations may be given. 

Vasomotor disturbances are exceedingly frequent after nerve lesions, and 
are most striking after paralysis of the median nerve. In such, the second 
finger, sometimes the third or the thumb, exhibit violaceous discoloration. 
In ulnar nerve lesions, the fifth finger—somewhat less frequently the fourth— 
shows vasomotor signs and cyanosis. With palsy of the radial nerve, there 
is not the same restricted localization of the circulatory disturbances, but 
there is cyanosis of the whole of the dorsal aspect of the hand, and of the 
extensor surfaces of the fingers. Although the pendent position of the hand 
in the latter palsy may intensify the color, livid discoloration is not due to 
vascular obstruction. 

There seems to be an increased irritability of the vasodilators and a 
diminished response of the vasoconstrictors. Sometimes as a result of vaso¬ 
constrictor irritation, pallor is observed, occasionally a crimson red color. 
Subjectively the patients complain of coldness of the fingers and hands, and 
only rarely a prickling feeling of heat. 

Trophic disorders are cutaneous changes, particularly atrophy, hyper¬ 
trophy, ulcer formation, and alterations in the subcutaneous tissue. There 


NEUROSES AND THE PERIARTERIAL SYMPATHETIC NERVES 521 


are also changes in the fascia, bones and muscle; even anomalies of hair 
and nail growth. 

In the atrophic type of cutaneous change, the skin is smooth, thin, 
stretched and tense; it usually accompanies median nerve lesions. The 
other or hypertrophic type is more often associated with ulnar and sciatic 
palsy; and the skin is thickened or there is hyperkeratosis. 

Important manifestations of trophic disturbances are ulcers, usually 
small, indolent, and superficial, but that occasionally can penetrate into the 
depth and cause extensive necrosis. In ulnar lesions the tip of the little 
finger is usually affected, in median nerve lesions the tips of the second and 
third; in case of the radial nerve, ulcers are rare. But an area over the dorsum 
of the first metacarpal may be affected. Usually a slight burn or pressure or a 
trauma are the exciting factors in the production of the ulcers. 

After bullet wounds or other injuries of the nerves the following have been 
noted: Chronic articular conditions suggesting rheumatism; restricted growth 
of the phalanges of hands and feet, and bone atrophy. According to Lehmann 
the following points are characteristic of bone changes after injury to the 
nerve: (i) Bone atrophy; (2) atrophy whose intensity is in proportion to the 
degree of neuralgia; (3) atrophy that is not explicable through the degree of 
inactivity; (4) atrophy localized particularly in the region of the epiphyses and 
the heads of the bones, the diaphyses remaining unchanged. 

Vasomotor Symptoms in Infectious Polyneuritis. 1 —In severe cases of 
polyneuritis following grippe, sensory, vasomotor, and secretory disturbances 
may be sequelae. Hyperhidrosis with rubor and a turgid condition of the 
skin of the feet and legs has been reported. During the paralytic stage 
increased warmth and reddening of the skin of the hands and marked sweating 
are derangements that are described as running parallel with the motor 
deficiency symptoms. 


CHAPTER XCII 

NEUROSES AND THE PERIARTERIAL SYMPATHETIC NERVES 

There are clinical complexes in which vasomotor symptoms play but a 
subsidiary part, and that have been latterly attributed to peripheral, peri¬ 
vascular, sympathetic nerve derangements (French school). A short refer¬ 
ence to these may be made here to enable the reader to clearly segregate the 
so-called true vasomotor from the trophic neuroses. 

We must remember that lesions of the peripheral nerves may present 
manifestations such as paralyses, sensory disturbances, anesthesia, hypo- 
or hyperesthesia, and pain; whilst lesions of the sympathetic system are said 
to evoke contractures, circulatory, as well as trophic disturbances. 

Observations made during the Great War have emphasized the fact that 
sensory disturbances may arise from two wholly different sources. For it is 
now believed that sensory impulses may have their origin in the sympathetic 
nerves within the realm of the vascular system. The causalgias are regarded 
as due to lesions in the sensory nerves; a combination of contracture and 
circulatory phenomena as referable to sympathetic nerve lesions. 

1 Klein, Wien. Arch. f. inn. Med., 1921, II, p. 329. 


522 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The Painful Lesions of the Sympathetic. 1 —The clinical picture of the 
sympathetic type of painful lesions is somewhat different. There is usually 
less pain than in the causalgias. The crises are absent, in that the patient 
is never so distressed that he fails to take care of his wants, nor does the pain 
interfere with his sleep. A feature that is characteristic, here, is the presence 
of contractures. In these there may be flexion of one or more fingers with 
fixation so intense as to be released neither through passive nor active force. 
In addition, there are noted circulatory disturbances, bluish or violaceous 
hands, and trophic disorders. Of the latter, ulcerations of the fingers may 
be mentioned. The radial pulse may be absent and there often is a history 
of ligation of the brachial artery. 

Combinations of irritative lesions of the sympathetic and lesions of the 
peripheral nerves may occur, usually with involvement of the median nerve 
that courses in the immediate neighborhood of the sheath of the brachial 
artery. In such cases the circulatory disturbances are localized in the cutan¬ 
eous territory of the median nerve in the form of violaceous discoloration of 
the hands, the territory of the ulnar and radial showing no such discoloration. 

As an example of contractures and circulatory disturbances, possibly of 
this type, the reader is referred to the second example of embolic closure of the 
brachial artery (Chap. LXXXV, p. 496)• Here, it is true, there was an 
infection after an embolectomy or removal of a clot and the contiguous nerves 
may have been implicated. It was in this way that the neurologists inter¬ 
preted the vascular and contracture phenomena. Nevertheless the clinical 
picture resembles rather those complexes which the French authors describe 
as caused bv disorders of the periarterial sympathetic. 

The Sympathetic Nerves in Relation to Causalgia.—Causalgia (a com¬ 
plex associated with peripheral nerve lesions) includes painful syndromes of 
focal types. Amongst the symptoms are constant pain, burning sensation, 
paroxysmal crises of pain evoked by the slightest touch of the part with an 
external object, or with something that is warm and dry. Only objects that 
are wet and cold ameliorate to a slight extent the acuity of the symptoms. 
In some cases all the usual physiologic acts, even the idea of performance, 
may provoke paroxysms of intolerable pain. 

In addition to the sensory symptoms there may be absolute functional 
impotence, but of such character that differentiation between actual paralysis 
and fear of execution of motion is difficult. 

Of some interest was the observation of Leriche 2 that certain extremely 
rebellious cases of causalgia, upon which no effect had been produced by 
division of the nerve in question, were at least temporarily cured by stripping 
the sympathetic fibers from the blood vessels below the nerve lesion. He 
concluded therefrom that the exciting cause of the manifestations was not a 
lesion of the nerve itself, but of the neighboring perivascular sympathetic. 

Causalgia according to certain French authors 3 is essentially a sympa¬ 
thetic symptom-complex, in which through a sympathetic reflex arc, there 
occur painful centripetal excitatioit and centrifugal reactions of the vasomotor 
form, and secretory or neurotrophic disturbances. These aid in prolonging 
and augmenting the pain. When the lesion of the nerve implicates sympa¬ 
thetic fibers, the point of departure of the painful sympathetic excitation can 
be anatomically found. In such a case relief from pain may be obtained by 
section of the nerve above the lesion. Where, despite this procedure, the 

1 These views of lesions of the French school must not be accepted as final. 

2 Leriche, Presse med., 1917, 25, p. 513. 

3 Tinel, Rev. Neurol, 1917, 243. 


TRAUMATIC VASOMOTOR SPASM 


523 


causalgia persists, it is assumed that there exists an irritation of the sympa¬ 
thetic terminations in the peripheral territory of the nerve. In such cases 
the painful sympathetic excitations, like the reflex responses, are conducted 
by the lateral, probably perivascular paths. These painful excitations induce 
a state of marked hyperexcitability in the sympathetic, diffusing into the 
neighboring centers, and even into the homologous centers of the opposite side. 
This condition (described as erythema) is accompanied by “synesthesalgia,” 
which is not infrequently restricted to the clinical “ causalgic field.” Modifi¬ 
cations in sensibility, especially a superficial hypesthesia by inhibition or 
even blocking of the sympathetic, may be observed in quite a large sympathe¬ 
tic field. Profuse sweating, mydriasis and vasodilatation, evidences of 
diffuse sympathetic reaction, are noted in distant parts. 

For the sympathetic origin of causalgia, the French school adduce con¬ 
firmatory evidence. 1 Contractures have been observed as the dominant 
findings in painful affections of the limbs, and with these, lesions of the 
periarterial sympathetic were repeatedly encountered. In these periarterial 
sympathectomy is said to have afforded relief. 

Without reflecting on the correctness of the therapeutic results obtained 
after the operation of periarterial sympathectomy or decortication, it is 
noteworthy that anatomical and physiological facts do not offer a satis¬ 
factory explanation for these. Leriche assumes—and the rationale of his 
procedure is perhaps based thereupon—that the majority or all of the vaso¬ 
motor fibers course in the sheaths of the larger arteries in uninterrupted paths. 
It has been elsewhere shown that this is not the case. The effect of the 
operation could not altogether be due to an interruption in the continuity 
of these fibers. Perhaps reflexes engendered, however, may be responsible 
for some of the consequent alterations of innervation. 

Treatment.—Three types of treatment are applicable for these diverse 
clinical complexes. On the one hand, for relief of the causalgias, the nerves 
involved—such as the median, sciatic, popliteal—require our attention. 
Interference with the conduction of pain impulses to the higher centers may 
give relief. Intramural injections of alcohol, or injection of other substances 
such as novocain and saline solutions, have been suggested. 

In the irritative manifestations of the sympathetic type Leriche has 
suggested periarterial sympathectomy. Finally, electrotherapy and physio¬ 
therapy of various forms are valuable adjuvants. 


CHAPTER XCIII 

TRAUMATIC VASOMOTOR SPASM 

Clinical observations made during the Great War have emphasized the 
importance of recognizing the occurrence of local vascular spasm of traumatic 
nature. It had already been noted by the author in 1910-1911, and by 
numerous observers since, that exposure of an artery, such as the radial, for 
purposes of direct transfusion was frequently followed by such intensive 
spasm that no blood would flow through it. Similar arterial spasms may 
develop when wounds are inflicted in the vicinity of large vessels. Such 

1 Girou, Presse med., 1918, LXIII, 584. 


524 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


vessels on excision may be found completely patent, even though pulsations 
had been absent. 

The following observation of Kiittner and Baruch 1 is a typical one. 

A soldier (Aug., 1916) received a number of injuries from a hand grenade. On the 
outer side of the Achilles tendon of one leg there was an irregular bullet wound of entry, 
immediately above the heel. There was no arterial bleeding, although venous blood oozed 
from the wound. 

Operation was done 4 hours after the injury, and the wound of entry and exit were 
excised. The Achilles tendon and bone were found intact. The posterior tibial vessels 
were exposed after excision of the bullet tract. The posterior tibial vein was torn and the 
injured portion resected and vein ligated. The posterior tibial artery was found uninjured , 
although there was some inhibition of the adventitia with blood where it was in contact 
with the vein. Pulsation in this part of the artery was absent. On dissection of the artery 
it was found that pulsation was strong above, whilst towards the periphery all pulsatile 
excursions were absent. 

The diagnosis of thrombosis was made. About 2 ^ cm. of the non-pulsating portion of 
the artery was removed, and ligation done. Immediately upon resection of this region , the 
peripheral portion began to pulsate. 

Examination of the artery showed that thrombosis was absent, the intima was intact 
and the vascular wall normal. 

Kiittner and Baruch report 23 cases of traumatic vessel spasm. Other cases are 
reported by Abadie, Delbet, Fiolle, Leriche and Tuffier. 

The clinical course and the causal mechanism in these cases have been 
illuminated by the recognition of a special morbid syndrome. This comprises 
more or less complete interruption of the circulation of a member through 
traumatic irritation of the region of the supplying artery, usually unattended 
with organic arterial alterations of any significance. 

In the severe cases gangrene may occur. The peripheral pulses are absent 
and the affected extremity is cold and blanched, having a yellowish or slightly 
bluish tint. There are sensory disturbances, either absent or diminished, 
and active motility is impossible or motion is carried out with great difficulty. 
When this condition lasts for many hours, the outcome in gangrene is so 
certain, that some of the authors have recommended early amputation. 

Leriche 2 reports cases in which the arm was limp and lifeless, and the 
fingers colorless so as to give the impression “that the brachial artery was 
crushed.” In these the mainfestations were of temporary nature. 

Although threatening gangrene is occasionally observed, no case of 
absolutely authoritative example of true gangrene following protracted 
spasm of arteries (traumatic) can be found in the literature. There are 5 
cases (Kiittner, Baruch) in which gangrene was expected, but in which 
restitution occurred even though threatening symptoms were present from 4 
to 12 hours. 

In cases of moderate severity, the only striking sign may be an absence of 
peripheral pulse, suggesting the diagnosis of a solution of continuity in the 
supplying artery. 

In the mild cases we may group those in which the peripheral pulses are 
still present, although diminished. The qualitative differences may be such as 
to require the use of a blood pressure apparatus for differentiation. 

Another symptom referable to vasoconstriction is an unusual sort of 
burning pain. It may persist for months or even a year, may be continuous 
or return in paroxysmal crises together with painful hyperesthesiae. 

Pathogenesis.—The characteristic pathologic change in 20 cases was the 
constriction of the affected arteries. Although it must be admitted that 

1 Kiittner and Baruch, B run’s Beitr. z. klin. Chir., 120, p. 1. 

2 Leriche, Ann. Surg., LXXIV, 1920, p. 388. 


TRAUMATIC VASOMOTOR SPASM 


525 


similar observations on small arteries might be inaccurate, it is the large 
arteries that are usually affected (common carotid, brachial artery, posterior 
tibial). The spasm usually is localized over an area of from 2-5 or 10 cm. 
in length. The transition from the narrowed to the normal portion is a 
sudden one, where the delimitation is evidenced by a narrowed zone. The 
pulse wave encounters here a more or less insurmountable obstruction, so 
that the artery beyond the ring of spasm is pulseless and motionless. Only 
in one case where operative demonstration of this phenomenon was reported 
was a peripheral pulse palpable. 

Three cases are reported in which the exsected and opened artery was 
absolutely normal, the intima being intact, the adventitia presenting merely 
localized hemorrhagic infiltration. It has been conclusively proven that 
this spasm can occur without anatomic lesion of the arterial wall. 

In short, the gross anatomic changes do not throw any light upon the 
pathogenesis of this type of morbid entity. 

A number of explanations have been given for the causative factors in 
traumatic vascular spasms. Vascular contraction is explicable either through 
irritation of the vasoconstrictor nerves of the sympathetic, or through direct 
irritation of the vessel’s musculature. According to some, the mechanism 
that conserves the vascular tone lies in the vessel wall itself, and is merely 
regulated by the central vegetative nervous system. These believe, too, that 
an autonomic nerve mechanism, such as exists in the heart, can be attributed 
also to the vessels. 

Kuttner and Baruch, in the consideration of traumatic vascular spasms, 
lean to the view that the theory of myogenic origin can best explain the 
occurrence of localized vessel spasm of traumatic type. It is well known 
that most vessels react intensively to mechanical external stimuli. Thus, 
sudden changes in temperature cause vasoconstriction in vessels that have 
been robbed of their nerves. The manipulation incident upon the dissection 
of vessels for purposes of transfusion has demonstrated, too, that mechanical 
irritation produces local vascular constriction. 

It must be admitted that we have no absolute means of differentiating 
between the symptoms of impaired circulation due to local vasoconstriction, 
and mechanical interference with the patency of vessels. 

Prognosis.—As a rule, the outcome is good. However, because of the 
uncertainty, and the threatening nature of the symptoms, intervention with 
resection of the affected vessel has been frequently resorted to and deemed 
advisable. 

Therapy.—Resection, although done in some of the cases reported in the 
literature, should not be regarded as a correct procedure, since the absence of 
pulsation in a part of a vessel under observation does not necessarily imply a 
persistence of the phenomena. Some authors recommend irrigation with hot 
saline solution, others massage of the constricted portion of the vessel. 
The subcutaneous injection of atropin should be tried. 

Decortication and Peri-arterial Sympathectomy. —Leriche 1 reported interesting results 
after interrupting the sympathetic pathway in arteries of the limbs by decorticating the 
vessel for a distance of about 8 to 10 cm. Horrax states that two distinct reactions followed 
such procedure, one, lasting for 6 to 12 hours, consisted in a contraction of the artery to 
one-quarter of its former volume over the decorticated area, feeble or imperceptible pulse in 
the extremity, and a lowering of the surface temperature of the limb. The other reaction, 
lasting for 2 weeks to a month, consisted in an elevation of 2 to 3 degrees of the surface 
temperature of the limb. This procedure has also been recommended, although insufficient 
data are yet at hand to give it a definite recognized value as a therapeutic agent. 

1 Leriche, Soc. med. des hopitaux de Lyon, Dec. 2, 1919; Lyon, med., Jan. 10, 1920, 40. 


526 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER XCIV 

LOCAL SHOCK 

Local shock is an appellation given to certain vasomotor and sensory 
phenomena caused in an extremity by trauma. Since there are marked 
vasomotor disturbances with noticeable changes in the pulses of the affected 
limbs, a knowledge of this symptom-complex belongs to the domain of the 
morbid conditions discussed in this treatise. 

Characteristic manifestations are local derangements of motility, sensi¬ 
bility and circulation—these being evidences of a local depressive state. Such 
a condition is said to result from local shock of the peripheral nerves, although 
this explanation is not altogether convincing. According to Seydel, 1 a bullet 
tract and its surrounding parts may be found insensitive. Or, this condition 
may spread over a larger territory so as to implicate the whole or a large 
part of the limb, or corresponding section of the body. v. Mosettig describes 
the limb affected as being cold, its skin pale or bluish, the part paralyzed and 
without sensation. Indeed, patients may have the impression that the part 
is absent, having no sensation therein. At times there are formication and 
other paresthesiae. 

Wieting 2 observed cases with somewhat different symptomatology during 
the Great War. In these, after severe exposure or after intensive contusion 
of one or both lower extremities, striking manifestations were noted. 
Besides the immediate results of the trauma, which was in no case an open 
wound, the limbs were found immobile and pulseless. With this there 
were the symptoms of severe shock except for a relatively slight accelera¬ 
tion of the pulse. Within 48 hours or in a very few days, death ensued. At 
autopsy the internal organs were found normal. It is true that the muscles 
of the contused extremities were extensively lacerated, showing degeneration 
and white and hemorrhagic foci. Possibly autolytic tissue changes and 
resorption of toxic substances were factors in the clinical manifestations. 
Some of the cases recovered. 

Pathogenesis.—A reflex nerve mechanism through the spinal cord is 
regarded as being at play in local shock. The insult probably stimulates the 
peripheral nerves throughout. Impulses from the whole cross section of the 
limb are then transmitted to the spinal cord by way of the sensory nerves, and 
sympathetic cord. Granted that a “ shocked ” condition of the reflex arc may 
be produced by trauma, then a paralytic vasomotor effect must needs occur. 
There is never isolated participation of single nerves, even of considerable 
size; but all of the nerves at the injured level are involved. 

The gradual transition of local to generalized shock, however, is a pheno¬ 
menon that has not been adequately explained. How does a local vessel 
palsy, become ubiquitous after abatement of the exciting traumatic cause? 

Diagnosis.—The early local signs of gas bacillus infection when deep 
seated may be mistaken for local shock, all the more so since the limbs, 
already in the condition of local shock, were found especially prone to 
this type of bacterial invader. 

Immediate injury of peripheral nerves, or lesion of such without ana¬ 
tomical alteration, must be excluded. Characteristic for the latter is the 

1 Seydel, Lehrbuch d. Kriegschirurgie. 

2 Wieting, Ergebn. d. Chir. u. Orth., 1921, 14, p. 656. 


CHRONIC ACROASPHYXIA 


527 


fact that the symptoms are confined to the territory supplied by the affected 
paths, whilst in so-called local shock, the territory involved extends from its 
inception at and about the wound or traumatized zone, in every direction 
until the whole limb is implicated. 

Critical Observations .—The remarkable sequence of local shock giving 
way to generalized shock with frequent lethal outcome would tend to 
substantiate the toxic theory of shock; namely, that certain forms of the latter 
are due to the action of toxins arising in injured tissue. This view is further 
upheld by the following observations: that removal of the injured region 
may cause the symptoms of shock to disappear; 1 and that the application 
of a tourniquet as tightly as [possible around a limb that was so badly 
contused that amputation seemed unavoidable, was followed by immediate 
improvement (McNee, Sladden and McCartney 2 ). 

These together with similar observations offer a suggestion as to treat¬ 
ment in local shock, wherever severe and irretrievable damage of an ex¬ 
tremity has been sustained. 


CHAPTER XCV 

CHRONIC ACROASPHYXIA 

This is a clinical syndrome to which some of the Continental authors 
have called attention—a clinical complex of neurogenic variety, that may 
easily be confused with some of the forms of organic vascular disease of the 
extremities. 

Characteristic of acroasphyxia chronica is the slow development of 
cyanosis or asphyxia of the terminal portion of the extremities. These 
manifestations are not unlike those attending Raynaud’s disease. There is, 
however, this difference, that paroxysmal attacks are absent. Associated 
with this manifestation there are other symptoms of trophic and sensory 
nature. Or there may also be present a neuropathic diathesis or other nerve 
malady. 

Cassirer was the first to group these cases under the caption “Chronic 
Acroasphyxia.” Whether all the cases previously described with their 
manifold deviations are correctly classed as an entity under this appellation, 
and just what their relationship to Raynaud’s disease is, has not yet been 
satisfactorily answered. 

In one of the usual forms there is acrocyanosis unassociated with pulmon¬ 
ary or cardiac disease, the discoloration developing rather suddenly over a 
period of a day or several weeks. A peculiar hypesthesia seems character¬ 
istic. The sensory symptoms do not appear to be of hysterical nature, 
although evidences of a general neurotic habitus are present. 

The following brief history is rather typical of the disease. 3 

A young woman of 19 years gave a history of tendency to frost-bite and to the develop¬ 
ment of painful fissures. Two weeks ago the hands began to be discolored, dark bluish red, 
there being sensation of prickling in the affected parts. Pallor or blanching was absent, the 

1 Cannon, Arch. Surg., 1922, 4, p. 1-22. 

2 Cited by Cannon. 

3 Cassirer, Vasmot. trophisch. Neurosen, Berlin, 1912. 


528 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


discoloration taking on a progressively darker hue. Pain, too, was absent, but a feeling of 
lack of sensation attended with prickling and tingling was experienced. Amongst the more 
remote symptoms were headaches, increasing nervousness with exaggerated sense of fear. 

Examination showed bluish red discoloration of the distal portion of both hands. The 
fingers were dark red throughout, with a bluish tint over the dorsal part of the hand extend¬ 
ing almost midway up to the wrist. Hyperhidrosis was distinct, the hands being cold to the 
touch, this coldness extending up to the forearm. Except for old scars and fissures, the skin 
of the hands was negative. The feet also showed a certain degree of cyanosis, but to a less 
marked degree. The cyanosis of the upper extremities was roughly symmetrical, there 
being a slight difference in the intensity of the discoloration. Associated with these 
symptoms was a distinct diminution in the sensibility over the affected parts. All of the 
sensory qualities were involved. The limits of the hypesthesia could be distinctly demar¬ 
cated in a line roughly perpendicular to the long axis of the limb. 

This condition lasted for months, the coldness and cyanosis persisting even in a warm 
room. On immersion of the hands in cold water, the bluish color became much darker. 
Local syncope was noted at no time. Pain was absent, and the paresthesiae were of but 
slight degree. 

The feature of this clinical picture is the bilateral peripheral acrocyanosis 
of both hands, developing rather rapidly within two weeks. The hypesthesia, 
neurotic symptoms, and a susceptibility to chilblains are also noteworthy. 
To this type the name, “ acrocyanosis chronica anaesthetica , ” has been applied. 

If we compare this affection with Raynaud’s disease which it resembles 
most, we find the same localization, but the absence of syncope. This alone 
would not sufficiently differentiate it from Raynaud’s disease, since even 
blanching may be absent in the latter malady. However, the absence of 
pain , as well as of the paroxysmal attacks and the progressive develop¬ 
ment of cyanosis, are real distinguishing criteria. Indeed, paroxysmal attacks 
are pathognomonic of Raynaud’s disease. The anesthesia of this type of acro¬ 
cyanosis is also rather suggestive, for it is rare in the Raynaud complex. 

Another interesting observation of this nature is reported by Barker and 
Sladen. 1 The history may be summarized as follows: 

A male, 44 years of age, began some 10 years previously with the present condition, the 
onset being characterized by cramp-like pain in the leg that would come and go. This, 
however, disappeared after 5 years. Then there occurred multiple attacks of numbness of 
the fingers without discoloration. Subsequently and gradually came a feeling of numbness 
in the toes of the feet, and latterly, a bluish red discoloration with nutritional disorders of 
the skin and nails developed, but unattended with any painful sensation. 

Physical Examination. —Both feet and part of the legs were cyanotic; the pedal arteries 
pulsated; the first three toes of the right foot showed ulcerations; and there was a large ulcer 
over the plantar aspect of the big toe. There was also cyanosis of the hands up to the wrist. 

In short, 6 weeks after the first observations were made, the picture was as follows: 
marked cyanosis of the right foot, less of the left; the hands cold and cyanotic without 
syncope even after dipping into cold water; all the arterial pulses present, the trophic 
disorders disappearing after removal of the distal phalanges of the first and second toes 
(right). 

The authors summarized this case as characterized by (1) cyanosis and 
swelling of the soft parts; (2) paresthesia and anesthesia that do not corre¬ 
spond to the distribution of any nerve; (3) absence of pain; (4) dystrophic 
disturbances in the skin and bones, localized to the fingers, toes, feet and 
lower extremities; and (5) with a chronic progressive, and not a paroxsymal 
course. 

Acroasphyxia Hypertrophica with Marked Trophic Changes.— A certain 
group of cases, in which besides the asphyxia there are distinct trophic 
disorders of the soft parts, have been classified under this caption. The 
clinical picture has a certain resemblance to acromegaly. One of Cassirer’s 
cases will illustrate: 

1 Barker and Sladen, Jour. Nerv. and Ment. Dis., 1907, p. 745. 


CHRONIC ACROASPHYXIA 


529 


A male 42 years of age had been well until 1904, when, after a fall, he passed into a stage 
of chronic suppuration lasting some years. In the course of the next year and a half he 
had a number of foci of osteomyelitis. Then there came the gradual changes in the hands 
and feet. It is of these that he complained when the history was: 

The color of the hands gradually became more and more blue without attacks of syncope, 
and the hands also became awkward. Enlargement of the hands then took place, so that he 
could find no glove to fit him. Because of the coldness of the hands, gloves were necessary 
and these had to be made to order. The sensibility of the hands too diminished, particu¬ 
larly to warmth, hot water. There was no pain at any time. 

Later his feet also showed similar, but less pronounced, changes. No alterations were 
noted in the face. 

Physical Examination. —A powerful man with normal organs. The hands are totally 
discolored, bluish with isolated red and cyanotic patches. The color change reaches 
intensively up to the wrist, and from there on in diminished tints up to the lower limit of the 
middle third of the arm. The temperature of the skin is diminished irregularly; the hands 
markedly enlarged, plump. The dorsal and solar aspects look padded, the skin being 
devoid of induration. The latter is rather soft and succulent. The fingers are sausage-like 
by reason of their enlargement, the distal phalanx about as thick as the first. 

All the arteries of the hands and legs pulsate normally, including the brachial and 
femoral arteries. There are no changes in the motility and electric reaction. Sensory 
disturbances are demonstrable especially in the diminution of the temperature sense. In 
the roentgenogram the bones are intact, the enlargement being limited to the soft parts. 
No evidences of acromegaly are present. 

Other instances have been reported, in which acromegaly is said to be 
associated with an atypical Raynaud complex. When the usual symptoms 
of acromegaly are absent, they belong more properly in the class of chronic 
acroasphyxia hypertrophica. In a number of such cases, the following 
characteristic symptoms of acromegaly were absent, namely, headaches, 
enlargement of the lower jaw, visual disturbances and kyphosis. In acro¬ 
asphyxia the bones are not essentially implicated, and the vasomotor dis¬ 
turbances may precede the trophic alterations by a considerable period of 
time. 

The Mild Form .—In the less intensive form, this affection is more fre¬ 
quently observed. There may not be any parallelism between the intensity 
of the vasomotor and trophic derangement. The latter are more apt to be 
minimal or almost absent. 

In a case of Oppenheim, a woman 31 years of age, the fingers of both hands were deep 
reddish blue, the hands less cyanotic. The skin of the fingers was smooth and soft, with no 
indication of sclerodactyly. The sensibility was intact, the nails without change. 

In the above instance in spite of a rather long duration (13 years), the 
nutritional changes in the hands were very slight, although there had been 
permanent asphyxia for a long time. 

More frequently the acroasphyxia is associated with but very slight 
enlargement of the terminal phalanges without osseous changes, the sub¬ 
cutaneous connective and fatty tissues only being involved. The hands are 
diffusely red and cyanotic, cold and somewhat moist. They may seem large 
and extraordinarily soft. The compression test or circulatory return in the 
skin demonstrates rapid reflux. 

Such cases are not uncommon, and have been explained as due to thyroid 
malfunction. 

Acroasphyxia and Acromegaly. —These have been reported as not infre¬ 
quently associated in several cases. Even a symptom-complex (Oecono- 
makis 1 ') in which acroasphyxia, acromegaly and gigantism are combined 
has been described. Chvostek and Bonardi cite similar combinations. 
Chronic local asphyxia in such cases is believed to be due to malfunction of 
1 Oeconomakis, Neurol. Centralbl., 1917, 36, p. 578. 


34 


530 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the hypophysis, either by virtue of direct action or through the nerve 
centers. The possibility of diffuse glia hypertrophy in the central portion 
of the vasomotor apparatus had been suggested by Cassirer as a possible 
cause, as a parallel hyperplasia of neuroglia tissue has been believed to 
exist elsewhere in the nervous system in acromegaly. 

The hypertrophic changes do not seem to be dependent upon the vaso¬ 
motor, since they may precede or appear simultaneously. Oeconomakis 
assumes that in this case (one of acroasphyxia chronica anesthetica), there 
was a combination of acroasphyxia chronica anesthetica and acromegaly, 
and that furthermore the manifestations could be referred to a proliferation 
of glia tissue in the central vasomotor apparatus. 

Acromegaly and Gigantism.—A man of 21 years of age developed dull pain 5 years before 
observation, prickling sensation at the tips of the hands and feet, then also at the tip of 
the nose and ears, this soon followed by a purplish or dark violaceous discoloration. With¬ 
in 3 weeks the present condition of complete and persisting cyanosis had been brought 
forth. Simultaneous with the appearance of the cyanosis there was a progressive enlarge¬ 
ment of the hands, the pain and paresthesiae disappeared, but the cyanosis and enlargement 
remained. Associated with the asphyxia was a corresponding diminution of sensation 
to touch, pain and temperature; in short, the symptoms of acroasphyxia chronica 
hypertrophica. 

As for the signs of gigantism, these were evolved simultaneously with the cyanotic 
discoloration. Not only did the hands become larger, but a generalized increase in size 
was noted. The osseous changes were a general dystrophy with destructive and atrophic 
changes, particularly of the feet and the terminal phalanges of the toes.. The broadening of 
the maxillary and frontal sinuses, unusual enlargement of the occipital protuberance, 
and an irregular thickening of the cranium, were some of the manifestations and signs of 
acromegaly. 

Diagnosis.—1. Acrocyanosis chronica anesthetica is not easily confused 
with Raynaud’s disease. The two maladies are similar in the localization 
and the type of cyanosis. The intensity of the pain, the absence of 
paroxysms, and the gradual development of the cyanosis are characteristic 
for acroasphyxia. Anesthesia, too, is but rarely encountered in Raynaud’s. 

The sensory disturbances may simulate those of syringomyelia, but the 
complete absence of motor and trophic disturbances distinguishes it from 
that affection. 

From vasomotor phenomena polyneuritis it differs in that sensory, irrita¬ 
tive phenomena are absent, also motor, irritative and paralytic manifestations. 

2. In the chronic hypertrophic form , the chronic progressive course of 
asphyxia, and the gradual increasing volume of the parts are characteristic. 
Only the less pronounced cases may be confused with Raynaud’s disease. 
Differentiation must be based upon the following points: the absence of 
gangrene, the minimal intensity of pain, the absence or rare appearance of 
local syncope, the permanency of the cyanosis and increased volume of the 
parts. All of these speak for chronic asphyxia and against Raynaud’s dis¬ 
ease. The extent of the cyanosis is especially noteworthy in that the hands 
are most intensively involved, the color change is permanent, involving the 
forearm to its middle or higher. The diminished temperature of the hand 
and the hyperhidrosis are other peculiarities. In contradistinction to the 
Raynaud syndrome the end phalanges are either negative or show distinct 
enlargement. The skin is not indurated but is softer than normal, is not 
adherent to the deeper tissues, and, by reason of its succulent appearance, 
is not unlike that often attending syringomyelia. 

These cases must also be distinguished from the chronic cyanoses that 
accompany the hypertrophic osteopathy of pulmonary type, and further¬ 
more from the polycythemias with enlargement of the spleen. 


ER Y THROMELALGIA 


531 


3. The mild chronic forms of acrocyanosis may escape observation because 
of the paucity and slightness of the manifestations. Atrophic forms must be 
carefully differentiated from scleroderma. These cases are very rare. 

4. Differentiation from Organic Vascular Diseases. —If we keep in mind the 
symmetrical nature of this affection, and the diffuse cyanosis, and if we 
remember the association of anesthesia with or without hypertrophy in other 
forms, the recognition of the malady will not be difficult. The two atypical 
varieties, that with atrophy and the mild form with cyanosis alone, may give 
rise to greater difficulties of recognition. 1 

5. The early vasomotor manifestations of thrombo-angiitis obliterans may 
be confounded with this affection at a time when all the usual vessels are found 
to pulsate. A typical case of thrombo-angiitis with cyanosis as a feature has 
been described elsewhere. In the latter the cyanosis may be restricted to the 
toes, not so frequently extending over the greater part of the foot; is not 
symmetrical and is usually associated with pain that becomes more and more 
intense with the degree of cyanosis. The asphyxia in thrombo-angiitis 
obliterans is not permanent until the stage of threatening gangrene is at 
hand. Then, restricted in extent and intensity to but a part of the foot or 
hands (usually toes or fingers) it is soon followed by trophic disorders or 
gangrene. Ischemia and rubor may be absent at this stage, and a con¬ 
siderable period may elapse before we can be absolutely assured of the organic 
nature of the malady. Nevertheless, the features already alluded to are 
characteristic enough to permit of differentiation. 

6. In the peripheral vascular thromboses , with or without atherosclerotic 
changes in the artery, acrocyanosis is usually limited to one or several toes, 
and is also not symmetrical, although both lower extremities may be involved 
at different times (p. 490). 

7. An asphyctic type of vasoneurosis usually confined to a toe, may be 
a manifestation complicating arteriosclerosis; it does not properly belong 
here (see p. 578). 


CHAPTER XCVI 

ERYTHROMELALGIA 

Weir-Mitchell in 1878 described an affection characterized by the par¬ 
oxysmal occurrence of pain } redness and swelling of the feet, under the desig¬ 
nation “erythromelalgia.” Hyperesthesia , motor, secretory and trophic 
disturbances may amplify the syndrome. 

1. The Pain. —The predominant symptom is a burning and sticking 
pain that may attain unusual intensity, oftened likened to the effect of “fire 
in the skin,” arising either suddenly with great severity, or gradually increas¬ 
ing from paresthesia up to a maximum degree. Thus from a feeling of prick¬ 
ling, formication, or numbness, pain seems to loom up augmenting until 
unbearable tortures that prevent sleep are oft experienced. 

Three factors influence the pain, the pendent position of the foot, heat, and 
exertion. Considerable diminution of the pain is brought about by raising 
the feet to the horizontal and keeping them at rest. 

The onset of the pain is described by Weir-Mitchell as in the foot, in the 
sole, or in the big toe, at times extending over the dorsum so as to involve 

1 Chap. CIV. 



532 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


more or less of the leg. Cassirer gives the following figures as to localization 
of pain: in both feet twenty-four times, in one foot nine, in both hands thir¬ 
teen, in one hand four, and in all four extremities, seventeen times. In the 
foot it is the toes, heel and sole; in the hands it is the fingers that are the sites 
of predilection for sensory disturbances. 

2 and 3. The Redness and Swelling. —Rubor may not appear simul¬ 
taneously with the pain but subsequently, for a period of sensory disturbances 
may antedate the advent of the discoloration by weeks or even months. At 
times redness, pain and swelling are coincidental in their onset. The color 
seems to be due to an active hyperemia, is a bright red, varying to a purplish 
hue attended with strong, bounding pulsations of the arteries and dilatation 
of the veins. Weir-Mitchell states that the active hyperemia yields to a 
passive stage, the arterial beating seems to abate, the bright red color changes 
to bluish red or violet with distinct manifestations of impaired oxygenation 
of the blood. Thus a variegated succession of colors from a bright red to a 
livid blue may be seen. 

The rubor is confined to the painful zones, usually the distal portions of the 
extremities, and the color returns rapidly after being made to disappear by 
digital compression. 

Accompanying this phenomenon there is often swelling of the skin that is 
transitory and evoked by the overfilling of the vessels. The temperature of 
the skin, too, is increased as has been demonstrated by actual thermometric 
measurements. 

As for the duration, this combination of symptoms is prone to come on in 
attacks that are incited by pendency of the feet, by heat or by exertion. We 
may distinguish two types, the recent and old cases. 

In the recent cases there are ordinarily no disturbances in the horizontal 
posture, but they appear immediately on allowing the limb to hang down. 
The local temperature rises, the arteries pulsate strongly, and the rubor 
becomes intense. 

The old cases , on the other hand, differ in that redness and pain are apt to 
persist in the horizontal position whilst the heightening of temperature with 
pendency is missing. 

The extent of the rubor corresponds within a somewhat restricted area to the 
seat of the pain, either delimited by a sharp boundary, or diffusely fading out 
into the normal. It is not exactly symmetrical since many variations and 
irregularities both in intensity and distribution are noted. Although it is 
the rule to find the so-called “acra” or peripheral ends of the distal parts 
attacked, cases in which a typical localization occurs are not infrequent, as 
in the elbows, knees, and forearm, without implication of fingers or toes. 

4. Hyperesthesia of the affected areas especially to touch is a fairly con¬ 
stant manifestation, the patients being unable to endure the slightest pressure 
on the affected parts, even the weight of the bed covers being unbearable. 
They are frequently unable to wear stockings and shoes, and even the milder 
cases must walk with the greatest care, bearing their weight on the unin¬ 
volved parts. 

5. Associated symptoms may be classified as: 

(a) Secretory disturbances. (c) Sensory disturbances. 

(b) Trophic disturbances. (d) Moltor distubances. 

(a) Secretory disturbances in the form of hyperhidrosis are not uncommon, 
over the palms, and soles of the feet, and, in general, corresponding in site to 
the rubor and pain. Profuse local perspiration coincidental with attacks of 
pain is a phenomenon reported by Weir-Mitchell and others. 


ER Y TH ROM EL A LGIA 


533 


(b) Trophic Lesions. —These are said to occur in somewhat less than one- 
third of the cases. Thus, (i) blebs of lentil or split-pea size on a reddened 
base that heal, giving way to others in various situations; or desquamation 
of the skin of the ball of the thumb following bullae formation; (2) thicken¬ 
ing of the skin not due to edema but to vascular dilatation and possibly 
connective tissue proliferation; (3) atrophy of the skin, the latter being 
smooth and fissured over an apparently enlarged phalanx, or parchment-like; 
(4) dystrophies of the nails and hair; and (5) rarely, in the late periods of the 
disease, gangrene 1 is a possible concomitant. This in its extent resembles 
that of Raynaud’s disease. Only very seldom has an early association of 
the trophic with the vasomotor signs been noted, so that a sufficiently long 
period is usually at hand in which the true nature of the disease may be recognized. 

(c) Sensory Disturbances. —The pain and sensitiveness to tactile irritants 
have been discussed above. Anesthesia and various degrees of hypaesthesia 
have been occasionally reported. 

(d) Local motor disorders such as paralysis with atrophy and reactions of 
degeneration in the territory of one or more nerves are absent. Simultaneous 
motor, sensory and vasomotor phenomena, however, have been observed 
when there is marked muscular atrophy. Weakness of the hands to the 
extent of an almost total loss of functional activity is cited by Weir-Mitchell. 

Other Coexisting Maladies. —As complicating the symptom-complex here 
described, it cannot be denied that other diseases, particularly of the nervous 
system, both functional and organic, may be coincidental. Cardiac affections, 
myxedema and osteomalacia also have been reported. 

Frequently a neuropathic habitus may be associated. Amongst the 
manifestations of the latter may be mentioned nocturnal emotional states, 
restlessness, attacks of vertigo, headaches, insomnia and nervous dyspepsia. 

Psychoneuroses too, melancholic states, and others are occasionally 
synchronous or prodromal morbid manifestations. 

Organic nerve diseases, such as antecedent cerebral hemiplegia, with 
symptoms on the paralyzed side, cerebral lues, paresis, tabes dorsalis, multiple 
sclerosis, and myelitis have been known to occur with erythromelalgia. 

In some instances, the symptoms seem to be restricted to the territory of 
one or more nerves without the presence of neuritic manifestations. Morgan 
reports a median nerve distribution; Weir-Mitchell, the posterior tibial; 
Oppenheim, the ulnar, and a number of other authors still different 
localizations. 

Pathogenesis.— As to whether erythromelalgia should be regarded merely 
as a symptom-complex associated with a number of diseases, or as to whether 
it deserves to be dignified into a morbid entity, is still a mooted question. 
Certain it is that similar manifestations, such as accompany obstructive 
arterial disease, when carefully studied will be found to present so many dis¬ 
crepancies from the Weir-Mitchell type as to require small powers of observa¬ 
tion for differentiation. 

Two distinct types of erythromelalgia exist: 

1. That in which the local symptoms follow the paths of certain nerves 

and 

2. That in which diffuse dissemination over certain peripheral parts 
occurs. 

Cassirer gives the following pathologic basis for these two forms: In 
the first group, we may assume an irritative process in the peripheral nerves 
with especial predilection for the vaso-dilator and secretory fibers, the sensory 
1 Bikeles, Wien. klin. Wchnschr., 1915, 30, p. 816. 


534 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


also being involved. However, the disparity between the true neuralgias 
and neuritides is adequate to justify a separation of erythromelalgia into a 
separate clinical entity. 

In the second group , the existence of a central nerve origin is a warranted 
assumption, the vasomotor, secretory and sensory elements being implicated. 
The sympathetic system is in all probability the seat of the disease. 

Clinical Course. —In the majority of cases a chronic progressive course 
is observed, more rarely the onset is sudden. The manifestations may remain 
stationary after having attained a certain degree of intensity and extent 
of distribution, or may even recede gradually. Quite a number of cases of 
improvement after several years’ duration are on record and in a few instances 
even cure after months or several years of manifestations. In general, a 
noteworthy degree of obstinacy is characteristic when the phenomena have 
become marked. 

The prognosis is therefore extremely dubious, complete cure being rare, 
improvement infrequent after months or years have elapsed. Quo ad vitam 
there is no danger from the disease, the lethal cases being those complicated 
by organic, cerebral, spinal, or cardiovascular affections. 

Diagnosis. 1 - —For the clinical diagnosis the two striking phenomena of 
rubor and pain are essential. However, it must be remembered that mere 
hyperemia in a limb that is painful or becomes increasingly painful when 
pendent is not a complex upon which the diagnosis of erythromelalgia should 
be made, for this association of rubor and pain is an almost pathognomonic 
feature of thrombo-angiitis obliterans, and may even attend arteriosclerotic 
vascular occlusion in certain stages of the affection. So we must separate 
what some have called a symptomatic complex similar to erythromelalgia 
from the essential , intrinsic form or true erythromelalgia. The former may 
accompany a number of other maladies and be not at all of vasomotor 
origin. 

The syndrome to be sought for in true erythromelalgia is a combination of: 

Active hyperemia , with the typical rubor , swelling and severe pain , occasion¬ 
ally also secretory and trophic derangements of paroxysmal appearance character¬ 
istically localized in the distal portions of the extremities. 

From thrombo-angiitis obliterans, differentiation should be easy if the 
peculiar features of the disease be comprehended. We may tabulate a 
comparative review of the two affections thus: 


T hr ombo-angiitis 

Arteries obliterated, do not pul¬ 
sate. 

Rubor constantly present also 
Intensified in pendent position; it dis¬ 
appears completely yielding to ische¬ 
mia on elevation. The redness dis¬ 
appears on digital compression, color 
returns sluggishly. 

Pain often intensified in pendent 
or elevated position. 

Swelling usually absent; in some, 
peculiar chronic puffmess that does 
not disappear. 


Erythromelalgia 

Arterial pulsation bounding, 
stronger during the attack. 

Rubor paroxysmal, intense in 
pendent position. On digital pressure 
disappearance, but rapid return of 
the color. Ischemia not demon¬ 
strable. 

Pain in attacks brought on by 
posture, intense, often unbearable. 

Swelling temporary associated 
and induced by posture. 


1 For the application of Capillary Microscopy in differential diagnosis, the reader is 
eferred to Chap. CVI et seq. 


ERYTHROMELALGIA 


535 


T hrombo-angiitis 


Erythromelalgia 


Symptoms of intermittent claudi¬ 
cation usually present. 

Trophic disturbances almost 
always complicate, often ulcers and 
gangrene; always associated with 
pulseless vessels. 

Predilection for young Hebrew 
males. 

Slow progressive course, first gan¬ 
grene of one, then often of other lower 
extremity, then possibly upper in¬ 
volved with amputation, a sequence 
in large percentage. 

Migrating phlebitis characteristic 
in a fair percentage. (Histological 
examination of extirpated veins yields 
characteristic pictures.) 

Most of the confusion existing in the literature in differentiation of true 
erythromelalgia from the symptomatic picture of rubor complicating other, 
particularly obstructive, arterial disease, is due to the publication in the 
literature of cases of erythromelalgia with arterial lesions. An analysis of 
these cases will show that none of them belongs to the true nervous affection 
“erythromelalgia.” 

Hamilton 1 seems to have misinterpreted the significance of occlusive 
changes in the peripheral arteries of a case; and incorrectly identifies the 
rubor or erythromelia with true erythromelalgia. Similarly others 2 are 
in error when they describe typical cases of thrombo-angiitis obliterans as 
being related to erythromelalgia. It is the redness in the dependent position, 
a striking symptom of thrombo-angiitis obliterans, and the pain that may 
lead the clinician to think of erythromelalgia; and the gangrenous termina¬ 
tion, which may cause confusion with Raynaud’s disease. Individual 
characteristic symptoms of thrombo-angiitis obliterans do not justify us in 
establishing a relationship between this disease and others in which some¬ 
what similar phenomena may be found. 3 


Intermittent claudication absent. 

Trophic lesions rare, come late, 
gangrene in type simulating Ray¬ 
naud’s, but vessels pulsate . 

Females and all races equally 
affected. 

Symmetrical distribution more 
frequent; prognosis better, amputa¬ 
tion almost unknown. 


Thrombo-phlebitis absent. 


The arteriosclerotic type of obliterative vascular lesion may present rubor 
and pain of either upper and lower extremities. The redness is usually not a 
vasomotor phenomenon but due to a chronic state of compensatory dilata¬ 
tion of the capillaries intensified in the pendent posture. It is frequently 
developed shortly after attacks of recent extensive arterial occlusion, that is, 
after thromboses; it disappears completely on elevation of the limb, being 
replaced by ischemia; its degree diminishes pari passu with such raising of the 
limb through an arc of 180 degrees. The expression test (digital compression) 


1 Hamilton, Jour. Nerv. andjMent. Dis., 1904, p. 217. 

2 Sachs, Am. Jour. Med. Sc., ,136, p. 562. . Hicpsmp* 

3 Similar misconceptions are found in the literature concerning Rayruud s* ^ease 
Me Am. Jour. Med. Sc., 1908, 136, p. 565, ™ which a typical case of tiro“bo-augims 
obliterans is referred to as follows: “It is worth noticing as etiological factors in this typical 
instance of Raynaud’s disease.” A careful study of this case will afford convincing proof 
that thrombo-angiitis obliterans was the lesion. See also the cases of Shaw (Brit. Med. 
Jour., March 21, 1903, p. 662), that are described as erythromelalgia, but belong to the 
organic vascular type of disease. 


536 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


is followed by an abnormally sluggish return of skin color and filling of the 
capillaries. 

Some of the arteries can always be demonstrated to be occluded. Other 
signs of arteriosclerosis are usually present. The affection is a slowly pro¬ 
gressive one and may lead to trophic lesions and extensive gangrene. 
Ischemia on elevation, a long history of intermittent claudication, with 
attacks of aggravation of symptoms due to thromboses, possibly previous 
ulcer formation with healing—all these are significant. 

Erythromelalgia with asphyxia and local syncope is a rare picture difficult 
to estimate correctly, and differentiation from Raynaud’s may be impossible. 

Erythromelalgia with marked trophic lesions will have to be regarded as a 
purely symptomatic concomitance of manifestations, when part of the picture 
is acromegaly, myxedema or scleroderma. The hypertrophy of the distal 
parts in true erythromelalgia is of a different order from that of acromegaly, 
in that bony enlargement is usually absent; then, too, the former affections 
present none of the typical alterations of the cranium, the cerebral symptoms 
(hemianopsia bitemporalis) of the latter. 

Neuritis and neuralgia with their distinctive features of paralyses, points 
of tenderness, etc., must be diagnosticated as such. In the absence of such 
pathognomonic signs, and where erythromelalgic symptoms occur in the 
territory of certain nerves, erythromelalgia of the first type with isolated 
nerve distribution should be diagnosticated. 

Miscellaneous obliterative conditions of the larger arteries of a limb may 
present the following complex: intensive rubor in the pendent position, pares- 
thesiae, pain, swelling of the fingers or toes, with or without trophic lesions at 
their distal ends. Such may be the manifestations of arteritis of infectious 
origin with occluding thrombosis; of luetic arterial disease with thrombosis; 
and either upper or lower extremities may be involved. In these affections, 
however, the radial, ulnar or brachial artery fails to pulsate, or the larger 
arteries of the foot and leg; ischemia can be elicited on elevation; the hand or 
foot is colder on the affected side, and varying degrees of atrophy are 
noteworthy. 

Therapy. —An endeavor should be made to mitigate the symptoms. This 
may be accomplished by placing the limb in a horizontal position, through 
the avoidance of motion and of exposure to excessive temperature changes. 
The best guide as to position will be the experience of the patient himself. 

Although cold is well borne by some, and cold water is occasionally 
employed by the patient to alleviate the symptoms, these may be aggravated 
thereby in other cases. Nevertheless the winter months seem to afford 
relief to some patients. 

Electrical therapy is of value at times; and faradic local baths maybe 
tried. The galvanic current with the anode over the painful part may be of 
some value. 

A large number of medicaments have been tried with very doubtful 
success; tonics such as arsenic, quinine 1 to improve the general health, the 
coal tar preparation for the pain, and sedatives for the neurotic manifestations. 
Suprarenal substance was suggested by Lewandowsky 2 and is reported by 
Moleen 3 as having been beneficial. Organo-therapy is not infrequently of 


1 Achard and Levi report recovery in a case following the use of this drug (Semiologie 
Nerveuse, p. 580). 

2 Lewandowsky, Quoted in the United States Dispensatory, Ed. 19, p. 583. 

3 Moleen, Jour. Am. Med. Assn., Aug. 17, 1912, LIX.j 


THE ACROPARESTHESIA 537 

value, if the existence of an endocrine dyscrasia in the case under consideration 
can be established. 

The Foerster Operation .—Resection of the posterior nerve roots is an 
operation suggested by Foerster for spastic paralyses, erythromelalgia and 
gastric crises. 

In a case of erythromelalgia reported by Mayesima 1 a favorable result was obtained by 
this method. The author describes the operation as follows: 

With the patient in the prone position, a median longitudinal incision was made from the 
ninth dorsal to the third lumbar vertebra, the spinous processes laid bare, the musculature 
displaced laterally, and the joints exposed. With the spinous processes and the laminae 
sufficiently removed, the posterior roots were brought into view. After splitting the dura, 
a longitudinal incision was made in the dura, the fourth and fifth posterior lumbar, and the 
first and second sacral roots exposed, and about i to i ^ cm. of each resected. Closure of 
the dura incision and suture completed the operation (no changes were found in the resected 
nerves histologically). 

In this author’s case, a young woman (24 years) suffering from erythromelalgia of the 
upper and lower extremities, the tips of the toes would become violaceous or red. The 
discoloration progressed centrally, becoming gradually more and more intensive and 
attended with increased local temperature. The toes, dorsum of the foot and part of the 
leg were involved, these areas being the source of exquisite pain. 

> About 5 months after the operation, the author reports complete absence of attacks of 
pain, heat and discoloration, but anesthesia of the right foot, and diminished sensation of 
the left. 

Opinions of the authors regarding various modes of treatment must be 
critically analyzed, since cases of organic vascular disease are not infre¬ 
quently mistaken for this affection. 


CHAPTER XCVII 

THE ACROPARESTHESIA 

This affection, first designated as acroparesthesia by Schulze, 2 but pre¬ 
viously described in somewhat different form by Nothnagel, comprises the 
following manifestations: 

1. Paresthesiae, such as formication, feeling of numbness, and creeping 
sensations. 

2. Pain of a tearing, variable character, not limited to the territory of a 
nerve. 

3. Disturbances of sensation including hyper- and hypesthesiae; and 

4. Vasomotor phenomena, such as coldness and pallor of the skin. 

In the variety of combinations presented not any one of the above symp¬ 
toms seems to take a dominant part in the complex, although there are 
acroparesthesiae without any of the other manifestations in some. Asso¬ 
ciated pain phenomena may play just as an important role in others. 

It may be of some clinical value to differentiate the cases of pure acro¬ 
paresthesiae from those attended with vasomotor or even trophic disturbances. 
The objective sensory manifestations of moderate degree may be present or 
absent in either of these forms, and so also may pain be wanting or a promi¬ 
nent symptom. 

1 Mayesima, Deutsch. Ztschr. f. Chir., Heft. 1 u. 2. 

2 Schulze, Deutsch. Ztschr. f. Nervenh., 1892, III, p. 300. 


538 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Haskovec 1 distinguishes 3 groups: (1) paresthesiae without vasomotor 
symptoms; (2) paresthesiae with secondary vasomotor, usually vasodilator 
symptoms, and sometimes trophic disorders; and (3) secondary paresthesiae 
with primary vasomotor changes (as in Nothnagel’s case). 

Clinical Course. —An observation described by Haskovec may illustrate. 

A woman 62 years of age complained that the right hand would “fall asleep” and would 
then become useless. Later, swelling of the wrist joint appeared with a. regional herpetic 
eruption. The fingers were reddened and slightly edematous. Objectively there were no 
sensory disturbances. Formication and creeping sensations, too, were complained of. 
After electrical treatment, the redness and swelling disappeared, but the paresthesiae 
persisted. 

In the cases of Nothnagel the sensation of numbness, a dead feeling with 
pallor, and coldness of the fingers were the characteristic manifestations. 

In 14 cases, all of which were females, there was usually a gradual development of 
paresthesiae (deadness and numb feeling) as if the fingers were absent, had fallen asleep, 
or were the seat of tearing pain and peculiar prickling sensation. The fingers, hands and 
anterior aspect of the forearm felt cold in varying degrees, and the tactile sensations were 
somewhat disturbed. Objectively there was diminished sensation to needle pricks, as well 
as to temperature and electrical stimuli. The disturbances were usually bilateral, and not 
confined to the territory of any nerve; whilst the mobility was unimpaired, except in so far 
as slight stiffness impeded the action of the fingers. The fingers were pale, white, and 
somewhat cadaveric in appearance. 

The symptoms were usually most marked in the morning and most prominent in cold 
weather; rubbing and hot water would bring about a certain amount of relief. 

Although the affection usually begins gradually, some instances of acute 
onset have been reported (Friedmann 2 ). Whilst in the latter the duration 
may. be only one or a few weeks, in most of the reported examples a chronic, 
recalcitrant type is described. In such the manifestations last months or 
years. 

The signs and subjective sensations are most marked in the morning. 
Some authors mention the effect of hot water in evoking the attack, and in 
rare instances cold. The carrying of objects, or the dependent position of 
the hand may incite the symptoms. 

Analysis of Symptoms. —Amongst the paresthesiae may be mentioned 
sensations of creeping, formication, itching, feeling of deadness as if the 
parts had fallen asleep; at times severe pain sufficient to awaken the patient 
and necessitate morphine. Such symptoms are apt to appear in attacks, 
either during the night or in the morning; during these the motility may be 
somewhat restricted. Usually both hands are involved; and more rarely 
the feet. The paresthesiae, however, are not confined to the territory of 
any peripheral nerve. 

Objective Sensations .—In most instances the sensory qualities are intact, 
although hyperesthesia and hyperalgesia have been reported. Cassirer 
mentions hypesthesia as being occasionally present. 

Motor symptoms are either absent, or of very slight degree. Some of 
the patients complain of irritative motor symptoms, such as contraction 
during the attack. The reflexes are normal. 

Vasomotor Symptoms .—Most of the recent authors describe cases in 
which paresthesiae and pain are combined, possibly with some slight sensory 
disturbances, while Nothnagel’s observations include instances of associated 
vasomotor phenomena. Local syncope does not properly belong to the 
complex acroparesthesia. Indeed, when the vasomotor symptoms become 

1 Haskovec, Wien. klin. Rundschau, 1897, 43. 

2 Friedmann, Deutsch. Ztschr. f. Nervenh., 1893, p. 450. 


GANGRENE WITHOUT ORGANIC VASCULAR DISEASE 


539 


prominent, we are dealing with a transition form between the acroparesthesiae 
and Raynaud’s disease. 

Pathogenesis. —The paroxysmal appearance of these manifestations 
would lead one to conclude that the responsible agent is one that must 
accumulate to produce its periodic influence. In this sense it resembles the 
neuralgias, except that in the latter intensive pain referable to the territory 
of certain nerves, and the painful points over the nerves with redness and 
hyperhidrosis are significant signs. Perhaps we can assume that there is an 
abnormal weakness of the nervous system that makes it unable to resist 
certain deleterious factors, and, indeed, it may be assumed that the vasomotor 
nervous system is here also in a condition of hypersusceptibility. Up to the 
present time explanations of the malady are based on hypothesis alone. 
Cassirer suggests that the sensory nerve endings, or those of the sensory 
vascular nerves, are affected; or that there is a disturbance of the vasocon¬ 
strictors, in view of the occurrence of cases with pallor and coldness. Accord¬ 
ing to this conception the acroparesthesia of the Schulze type (the simple 
form) represents a sensory neurosis; that described by Nothnagel a vasomotor 
sensory neurosis. In the former type the peripheral, sensory nerve endings 
of the skin and vessels are involved; whilst in the latter the peripheral, vaso¬ 
constrictor nerves are the seat of the disease. 1 In the latter the symptoms 
are brought about either directly or reflexly. 

Prognosis. —The disease may last for months or years without deleterious 
consequences; or the symptoms are acute and may rapidly subside. The 
health may be considerably impaired in the chronic variety. 

Therapy. —Treatment with electricity, especially Faradic current or 
Faradic hand baths have been recommended. Symptomatically these 
methods seem to be of some value. Hydrotherapeutic measures, including 
warm or cold local baths or douches of alternating cold and warm, have 
been rewarded with some success. 

Of the many forms of medication tried, the tonic treatment (including 
arsenic, phosphorus, and strychnin) is worthy of a trial. Quinin has been 
suggested, and arsenic is believed to be of special value for the vasomotor 
symptoms. 


CHAPTER XCVIII 

GANGRENE WITHOUT ORGANIC VASCULAR DISEASE 

There are still many clinicians who are of the opinion that gangrene of the 
extremities must depend upon some organic derangement of the patency of the 
arteries or veins, regarding those scant reports of Raynaud’s disease, in which 
changes in the vessels have been found, as being irrefutable testimony in 
favor of their own view. An analysis of such references in the literature has 
convinced the author that no distinct causal relationship between the 
vascular lesions and the symptoms has been definitely established in any of 
the reported cases. Furthermore, in the course of studies on arterial disease 
amputated material was obtained from cases of gangrene in which all the 
vessels were pulsating. Here an opportunity was afforded to prove conclu- 
ively that even extensive, spontaneous gangrene can occur without organic 
vascular disease. In order to dispel all doubt as to the possibility of the 
1 Miiller does not agree with the views expressed by Cassirer and would explain all the 
acroparesthesiae on a vasoneurotic basis. 


540 


CIRCULATORY AFFECTIONS OF TIIE EXTREMITIES 


occurrence of gangrene in the absence of vascular disease, and to clarify the 
concept of this type, the histories of pertinent cases are here recorded. 


Case I.— Sensory and Vasomotor Phenomena of Both Lower Extremities, Gangrene of 
Small Extent with Pulsating and Normal Vessels. M. R., male, Russian Hebrew, 40 years 
of age, was first examined by us on November 24, 1908. As far as can be elicited, there are 
no nervous stigmata; habits good, very little alcohol, smoking moderate. Some 6 years ago 
he remembers having had some “trouble” with both feet. There were periods of weeks 
and months during which the toes of both feet became exceedingly painful, the big toes 
being first affected, followed by successive involvement of each and every toe of both feet. 
He is not certain that the toes were discolored, but believes that they had a tendency to 
become blue. There was no pain in the leg and foot on walking. These symptoms would 
pass off after 2 or 3 months, and did not reappear for almost 9 months. He distinctly 
remembers a severe recurrence after this interval, but the relapse was not of as long dura¬ 
tion as the initial attack. He has been free from all symptoms for almost 4 years. 

In August, 1906, he was first attacked with severe pain in the middle toe of the left foot. 
The toe became discolored, intensely blue and slightly swollen. Gangrene set in within 3 
weeks and in September the toe required amputation. There had been no trouble in walk¬ 
ing or any ache whatsoever, nor can the patient think of any cause for the affection, such 
as injury, exposure, etc. 

In June, 1907, there was pain in the toes of the right foot, the fourth toe soon becoming 
blackish, an ulcer resulting after the separation of some mortified skin. 

In September, 1908, the middle toe of the right foot and the little toe of the left foot 
developed similar manifestations with small areas of gangrene. 

Examination, November 24, 1908.—Left leg: The third toe has been amputated at the 
first interphalangeal joint. The fifth toe is cyanotic over its distal half. Otherwise the 
color of the foot is normal. All the palpable vessels of the foot and leg, the dorsalis pedis, 
posterior tibial, the femoral and the popliteal pulsate strongly. Right leg: There is marked 
cyanosis of all the toes, particularly of the third toe even in the horizontal position. In the 
pendent position, the cyanosis gradually deepens, but absolutely no evidence of rubor or 
erythromelia can be elicited. In the horizontal position, the tips of the third, fourth and 
fifth toes are purple, but apparently less so than when examined some two weeks ago. 
There is a superficial patch of gangrene over the third toe, and the fifth toe shows the deepest 
blue discoloration. All the vessels pulsate, the dorsalis pedis, posterior tibial , popliteal and 
femoral. In the elevated position, it is difficult to determine whether ischemia is present or 
not. At any rate, it is not sufficiently marked to be diagnostic. In the pendent position, 
the right leg becomes more blue, the veins stand out very prominently and, at times, one 
can see a certain amount of rubor which is not typical of thrombo-angiitis obliterans. The 
same phenomena are present when the left leg is examined in this position; the pain becomes 
more marked, to such an extent that the patient cries for relief wishing to bring the foot 
back to the horizontal position. Sensation is practically normal over both feet and even the 
gangrenous toe has sensation, except over the mortified area. Nerve status, negative (no 
evidence of syringomyelia). Thus the symptom-complex is mainly characterized by 
cyanosis of the toes and foot, gangrene of slight extent with pulsation of all palpable vessels. 

On December 29 , 1908, the patient was again admitted to the hospital. He says that 
for more than a month the little toe of the left foot has troubled him, the bluish color per¬ 
sisting, till gangrene finally set in. 

Physical examination shows dry gangrene of the distal half of the little toe of the left 
foot. Now, too, the striking signs are the pulsation of the vessels, cyanosis and gangrene. 

January 4, the little toe was disarticulated and within a month the wound was healed. 

In brief, a case in which, after a prodromal period of attacks of sensory disturbances in 
the lower extremities, there supervened paroxysms in which sensory and vasomotor dis¬ 
turbances made their appearance. These in their turn gave way to dry gangrene, the toes 
of both feet being affected almost symmetrically. The absence of the typical ischemia, of 
erythromelia and of any evidence of obliteration of the vessels, excludes the diagnosis of 
thrombo-angiitis obliterans; we may, therefore, assume that we have here, either a case of 
atypical Raynaud’s disease or of so-called “acroasphyxia.” But even belonging to the 
latter it would be a variant form. 

Case II.— Paresthesice, Chronic Cyanosis , and Pain Terminating in Gangrene; All 
Palpable Vessels Pidsating. —M. S., 50 years of age, male, Russian Hebrew, admitted to the 
hospital February 13, 1909; traveling salesman; in this country 4 years. Habits good, smokes 
ten cigarettes daily, married, four children, denies lues. He "thinks that about 13 years 
ago, he had symptoms in the right hand similar to those that now affect his left leg. The 
finger tips were blue and cold, and there was a feeling of “pins and needles,” with occasional 
pain, lasting for almost 2 months. 


GANGRENE WITHOUT ORGANIC VASCULAR DISEASE 


541 


About 6 months ago his right leg began to trouble him, and the second toe became very 
blue, but the symptoms all disappeared upon internal medication. Three months ago he 
began to experience peculiar sensations in the toes of the left foot, and the third and fourth 
toes became very blue. In addition to the pain and cyanosis, there were peculiar sensations 
in the toes and in the ball of the foot, as if they were pricked by needles. As time went on 
these pains increased so that they finally became almost unbearable in the pendent posi¬ 
tion of the leg. As for the general symptoms, he complains of frequent dizziness, and 
attacks in which spots appear before the eyes. 

Physical examination: The patient is a well nourished male; heart negative; radial pulse 
somewhat thickened. Left leg: The third and the fourth toes are distinctly bluish, the 
foot is cold; all the palpable vessels are found to pulsate distinctly. Right leg: There is slight 
cyanosis in the pendent position. Wassermann reaction negative; blood varying between 
150 and 175 mm. Nerve status: no evidence of any organic nerve lesion can be detected on 
complete examination of nerve status. 

Examination, February 24: Left foot: Cyanosis of the left foot has considerably deep¬ 
ened in the horizontal position; the third, fourth and fifth toes are very blue, and on the 
plantar aspect suggest that these are the seat of the impending gangrene. The dorsalis 
pedis , posterior tibial, popliteal and femoral arteries pulsate strongly. There is slight edema 
of the forepart of the foot. 

March 4, 1909: Now the third toe of the left foot over its distal phalanx is distinctly 
gangrenous, the foot and ankle are very edematous, although all the vessels can be felt 
pulsating. There is no marked erythromelia, no marked ischemia in the elevated position. 

March 7: The second and third toes of the left foot are now completely gangrenous; the 
fourth toe shows a patch of superficial gangrene over its plantar aspect; the big toe is 
slightly cyanotic, but shows no evidence of gangrene. The edema of the foot is increasing 
considerably. 

In short, within a period of 4 months, the symptoms being cyanosis and pain in the 
left foot, there finally developed gangrene of three toes. Because edema was rapidly 
increasing over the foot and leg, and the gangrene bid fair to extend rapidly, and because of 
the intense, almost unbearable pain, it was decided to amputate, so that on March 11 the leg 
was ablated through the upper fourth. The larger vessels were found patent and required 
ligation. None of the usual appearances so characteristic of the vessels in thrombo-angiitis 
obliterans were found, and no evidences of thrombosis discovered at the point of section. 

On the following day, secondary hemorrhage occurred. The patient was taken to the 
operating room and the vessels caught and tied. 

On March 24, 1909, because of sloughing of the skin and absence of any tendency to heal, 
reamputation was done, after which the wound healed slowly, the patient being discharged 
on May 18, 1909. 

Summarizing the important features of this interesting case, we may say 
that in a patient in whom some thirteen years previously there has been a 
distinct history of vasomotor phenomena in the upper extremities, and in 
whom, some six months ago, the right lower extremity also seemed to have 
been involved in a similar way, there finally developed the following symptom- 
complex in the left leg: pares thesiae, pain and asphyxia or cyanosis of the 
left foot. After a period of four months, in which the pain became more and 
more severe, the cyanosis involving three of the toes deepened, finally ter¬ 
minating in gangrene. All of the vessels that can ordinarily be palpated 
were found distinctly pulsating and at operation proved to be patent at the 
point of ablation. 

The material from the case was particularly valuable for the pathological 
investigations. In Case I, the author was only able to obtain the little toe for 
examination; in Case II, however, the foot and lower two-thirds of the leg 
were carefully dissected and practically all of the larger arteries, veins and 
nerves preserved for microscopic examination, as well as the tissue of four 
of the toes. A thorough study of the larger nerves in Case II with the usual 
histological methods, was included in the microscopic research. 

In addition to the vessels of the toe in Case I the following arteries and 
their accompanying veins were completly dissected out in continuity in Case 
II, and a larger series of microscopic sections made: the posterior tibial, 
anterior tibial, the plantar arteries, dorsalis pedis, their venae comites, and the 


542 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


internal saphenous vein through their course, and all of the tissue save the 
bone of the second, third, fourth, and fifth toes. 

Except for slight thickening of the walls of the veins and arteries in a few 
places, and an occasional sign of the earliest atherosclerotic changes, the 
the vessels were practically negative throughout; nowhere were they occluded . 

Only few arteries leading into some of the gangrenous areas showed recent thrombosis, 
doubtless as a sequence of the mortifying process. Some interesting observations were 
made on the minute vessels in the subcutaneous tissues. Marked proliferation of capillaries 
was noted in places. 

The following nerves were examined: the internal and external plantar, 
the anterior tibial, the posterior tibial, and branches of the peroneal nerve. 
In none of these could degeneration be detected. The Marchi and Biel- 
schowsky were the methods employed in searching for degeneration. 

In short, there were neither lesions in the nerves nor in the arteries and 
veins that were in any way related, or could be held responsible for the gan¬ 
grenous process in either case. 


CHAPTER XCIX 

RAYNAUD'S DISEASE 

In spite of the extensive literature on Raynaud’s disease, the practitioner 
still finds great difficulty in recognizing this malady, and particularly in 
differentiating it from thrombo-angiitis obliterans. 

Raynaud in 1862 was one of the first to maintain that gangrene could 
occur without vascular occlusion in his monograph entitled “De l’asphyxie 
locale et de la gangrene symmetrique des extremites.” 

A careful clinical study of the various forms of sensory, vasomotor and 
trophic neuroses would suggest the recognition of a clinical group in which 
sensory symptoms (paresthesiae) predominate—as in the acroparesthesia of 
Schultze—and a group in which vasomotor and sensory phenomena are 
combined (Nothnagel’s acroparesthesiae). 

Whilst in some of the vasomotor neuroses to which Raynaud’s disease 
properly belongs—for example, in the simple acroparesthesiae (Schultze) 
and Nothnagel’s neurosis—sensory and vasomotor disturbances are the 
chief phenomena, and whilst in erythromelalgia, trophic disorders may be 
superadded, it is characteristic of Raynaud’s complex that neurotrophic 
alterations are amongst the most important features of the malady. 

Before entering into details we may clarify and facilitate our previous 
concepts by accepting the following clinical characteristics as those of a 
typical case. Cassirer concisely puts it as follows: 

Somewhere in the peripheral portions of the body {so-called acra ) there occurs 
more or less severe pain. This is not confined to distinct nerve territory, usually 
affects symmetrical parts. Attacks of vasomotor and trophic disturbances are 
part of the syndrome, to wit: (1) syncope, asphyxia, or local rubor, and (2) 
severe trophic disturbances, usually in the form of gangrene of the parts first 
affected with symptoms. The course is an intermittent one, for there may be 
completely free intervals; but in some instances, evidences of disturbed vaso- 
motility may persist. The disease may consume itself in_one attack or several 


RAYNAUD’S DISEASE 


543 


attacks may occur in succession. Objectively, sensory disturbances are usually 
absent, as well as paralysis , although other evidences of disturbed vasomotor 
innervation, aphasia, hemoglobinuria, and arthropathies, may occur. Usually 
neuropathic individuals are affected. 

Clinical Picture.— There is usually a story of psychic insult or exposure 
to cold in young women, and then the advent of the stage of local syncope, 
in which certain symmetrically situated peripheral portions of the body 
become ischemic and blanched. This gives way to a period in which periph¬ 
eral cyanosis is charactristic {local asphyxia). Or, a combination of both 
occurs, so that patches of whiteness and of lividity are contiguous. 
Accompanying these phenomena are paroxysms of pain, or, at times, anesthesia 
of the corresponding parts. Tingling, burning, formication and other pares- 
thesiae, with the substitution of lighter areas for the cyanotic patches, 
usually signalize the abatement and subsidence of an attack. 

Such cycles of symptoms recur at varying intervals until the symptoms in 
the milder cases completely disappear. In other patients, however, typical 
symmetrical gangrene develops. As the cyanosis deepens, the skin at the 
so-called acra (tips of fingers, toes, ears) becomes deep blue or almost black. 
Then dry necrotic areas of skin develop which scale off, the underlying parts 
receding so as to leave retracted scars. Although this is the typical clinical 
course and symptomatology, a great number of variations are encountered, 
in which either the syncope or the trophic disorders play an insignificant role. 

An interesting example of Raynaud’s, in which the diagnosis can be made 
although the clinical phenomena do not adhere in all particulars to the type, 
is the following case in which both upper and lower extremities were 
implicated. 

E. M., 54 years of age, female, believes she has had attacks for many years, possibly ten. 
Her feet and hands would get suddenly cold and white, the fingers and toes would become 
painful and then deep blue followed by red. 

Observation by the author on February i, February 2, and February 15, 1911, may be 
worthy of perusal. 

Feburary 1, 1911: The patient is in an attack, but believes it to be subsiding. Both 
hands are cold, the tips of the fingers red. The dorsal aspects of the second phalanges are 
very white. The color changes rapidly while the patient is being observed, the blanched 
portions becoming suddenly red. The fingers on palpation give a peculiar tense sensation 
as if moulded out of wax. The nails are deformed, and the second, third and fifth fingers of 
the right, and the third, fourth and fifth fingers of the left hand, at the tips, show scarring. 
The tip of the fifth finger (right) presents a large recent scar that is still tender. 

Both radials pulsate strongly. 

The vessels of the lower extremities are evidently patent. Almost all of the toes have 
patches of hemorrhagic discoloration that do not disappear on pressure, but at this time the 
feet seem to be free from an attack. 

February 2, 1911: The tips of the fingers are cadaveric; both radials pulsate well. 

February 15, 1911: The fingers of both hands show a mixture of cyanosis and extreme 
pallor and are very cold. As they are watched for a few minutes, a bluish discoloration of 
the third, fourth and fifth fingers comes on, and varies with alternating areas of rubor and 
pallor. 

The fingers of the right hand remain waxy and cadaveric. The nails appear white, the 
distal portions of the phalanges cyanotic. The dorsal surfaces of the second phalanges are 
blanched, the knuckles are cyanotic. Both radials pulsate during this period. A few 
minutes later the index finger of the left hand up to the first interphalangeal articulation 
becomes cyanotic and remains so, although color has returned into all of the other fingers. 
While the fingers were cyanotic, sensation was much diminished (almost absent) and 
returned on the advent of normal color. 

The tips of the toes were found livid. During a short period of observation there was a 
play of color over the feet, an interchange of cyanosis and rubor. 

A case approaching more closely to the classical description, although 
somewhat atypical, is the following: 


544 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Raynaud’s Syndrome in Young Woman , with Upper Extremities Involved. 

R. S., age 38 (referred Jan. 4, 1917), married nine years, three premature labors, one 
child born seven and a half years ago is well. 

Fourteen years ago she is said to have had severe dysmenorrhea, the ailment of which 
She now complains, and which involved her hands, appearing about that time. She believes 
that blueness and coldness of the finger tips particularly on exposure to low temperatures 
were the first noticeable changes. 

Then the attacks became more frequent, almost daily, with alternating blueness and 
pallor of the fingers of both hands, but unattended with pain until two years ago, when this 
symptom became an integral part of the malady. During each of three pregnancies, a 
remarkable improvement was noted, the attacks returning immediately after confinement. 

Simultaneously with the discoloration, a puffy condition of the fingers comes on and 
some changes have occurred in the skin at the tips. She has noted that whenever the 
symptoms in the extremities are most marked, gastric disturbances occur: such as vomiting 
of almost all ingested food; these would cease immediately upon the cessation of the attacks 
in the hands. 

Physical examination: All the fingers of the right hand are somewhat swollen, except 
perhaps the little finger. There is very slight puffiness of the fingers of the left hand. 
There are evidences of trophic disorder at the tips of the index and middle fingers of the 
right hand in the presence of small, dry, brownish scabs. The index finger of the right hand 
has a brawny feel, induration being distinct, and less marked over the tip of the middle 
finger, and still less over the tip of the ring finger. 

As the hands are watched, variations in color take place. At times the middle and 
index fingers of the right hand particularly become markedly cyanotic, the corresponding 
fingers of the left hand similarly affected but less so. A play of color takes place from time 
to time, cyanosis giving way to redness, which involves the greater part of the fingers 
affected. These changes take place so rapidly that a cycle of variations from blue to red 
and red to blue consumes a period of two or three minutes, or less. Spots of blanching 
appear from time to time. 

Pulses. —Radial and ulnar pulses are distinct. X-ray examination of the hands reveals 
a disappearance of the distal portion of the terminal phalanx of the index finger of the right 
hand; and a suggestion of incipient and similar changes in the left index finger. 

Lower Extremities.- —In the horizontal position there is slight cyanosis of all the toes of 
the left foot, most marked in the big toe, associated with some blanching of the proximal 
phalanges; the sole is cyanotic. Right foot is normal in color. 

Dorsalis pedis and posterior tibial arteries of both feet pulsate. 

Although many attempts have been made to cast doubt on the existence 
of the morbid entity of Raynaud’s disease, the author agrees with those who 
believe that an independent, intrinsic or idiopathic affection can be and 
should be recognized under that name. It is true that some of the manifesta¬ 
tions occasionally coexist as symptoms of other affections usually with central 
or peripheral nerve disease, but this is of relatively rare occurrence. This 
association has been noted especially with spinal cord tumors, syringomyelia 
and neuritis, also with a number of instances of psychoneurosis. When such 
is the case, we are dealing with a mere symptomatic coincidence that does 
not warrant the diagnosis of the true disease. 

Nomenclature.—Because the pathogenesis is so little understood, attempts 
to apply descriptive names have been unsatisfactory. Certain authors take 
issue with Raynaud’s descriptive title—“ Asphyxie locale et gangrene symme- 
trique des extremites on the ground that both asphyxia and gangrene may 
be absent. ‘‘Angiospastic gangrene” is criticized as implying the acceptance 
of a mechanism to which all authors do not subscribe. Thus, it may be 
best to adhere to the name “Raynaud’s Disease,” reserving such designations 
as “Raynaud’s Phenomena” and “Raynaud’s Symptoms” as denoting 
abridged, variant and incomplete pictures of the disease. 

Incidence. Age .—According to Raynaud, most of the cases occur 
between ages of eighteen to thirty years. Morgan 1 found an average of 

1 Morgan, The Lancet, 1889, H, P- 9 ff. 


RAYNAUD’S DISEASE 


545 


26.6 years in his ninety-three cases; Monro put this at 28.9 years. Of the 
hundred and sixty-eight cases collected by Cassirer there were fifty-five in 
the first and second decades as against forty from the age of twenty one to 
thirty years. In a subsequent study of a series of one hundred and nine 
cases Cassirer noted that the largest number of cases were from twenty-one 
to forty years of age. 

Sex .—Raynaud concluded that four-fifths of his patients were women; 
Monro found 62.6 per cent women, 37.4 per cent males; Cassirer obtained 
almost identical figures reporting 62.9 per cent females, 37.1 per cent males in 
180 cases. 

Statistics as to the relative frequency of the affection yield according to 
Monro 1 case to 3000 other affections. Of 7000 patients in the Neurological 
Clinic of Oppenheim, Cassirer found only 5 typical cases. It is more frequent 
than erythromelalgia, but more rare than the other vasomotor and trophic 
neuroses. 

Cold seems to influence the development of the disease and it has been 
observed to be of frequent occurrence amongst washwomen. 

Etiology. —A neurotic constitutional disposition of hereditary nature pre¬ 
disposes to this affection. Anemia sometimes seems to play a role, whilst 
in other cases, the general nutritional condition is excellent. Sexual and 
menstrual disturbances do not appear to be without influence according to 
Raynaud. 

Trauma has been held responsible (Cramer 1 ), so also psychic exertion, 
sudden fright, cold, wet, acute infections, and a neuropathic constitution. 

It will occasion little surprise that in a malady of such obscure pathogene¬ 
sis, the internal secretions should have been held in some way responsible. 
So we have a reference in the literature by Mobius 2 in the year 1896 to the 
possibility of the participation of the thyroid gland in the production of the 
syndrome. Solis-Cohen, too, has contributed observations and inferences 
bearing on the derangement of the internal secretions in the vasomotor 
affections. Leopold-Levi et de Rothschild 3 (1909) speak of para function 
(dyscrasia) of the thyroid. Voivenel et Fontaine 4 suggested the theory 
of hypothyroidism consequent upon ovarian insufficiency. 

Osborne 5 holds that Raynaud’s disease is not a distinct entity, but a 
syndrome caused by disturbances of one or more internal secretions; that it 
is not dependent on primary disease of the vessels, but that the vasomotor 
control is deranged in such a manner that most pronounced contraction of 
certain blood vessels may occur in different parts of the body; that such 
angiospasm may occur in internal organs as well as peripherally; that there 
is usually a disturbance of thyroid function; and hence the assumption is 
warranted and confirmed in his clinical observations that the administration 
of thyroid gland is followed by improvement in the majority of cases. 

The hypothesis that an increase of vasconstrictor substances in the blood serum may 
account for arterial spasm and gangrene in “so-called spontaneous gangrene’’ has found 
certain adherents (Oppel and Girgolaf 6 ); and a similar explanation has been invoked by 
some authors for the spasm in Raynaud’s disease. Hyperadrenalism or overactivity of 
the adrenals is believed to be responsible for the endocrine disturbance. 

1 Cramer, Arch. f. Orth., 1909, VII, p. 43 1 - 

2 Mobius, Vasomotorisch-trophische Neurosen, Penzoldt-Stintzing’s Handb. V Bd., I, 
Aufl., p. 472. 

3 Leopold-Levi et de Rothschild, Revue neurol., 1909, p. 209. 

4 Voivenel et Fontaine, L’encephale, 1910, II, p. 166. 

5 Osborne, Am. Jour. Med. Sc., Aug., 1915, p. 158 et seq. 

6 Chirurgitcheski Viestnik, 1922, No. 1, and Lancet, July 15, 1922, p. 116. 

35 


546 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Interesting as these hypotheses may be, incontrovertible evidence is 
still lacking to warrant unqualified acceptance of the endocrine nature of 
the disease. 

The influence of thyroid therapy on Raynaud’s disease has been emphasized 
by some authors as of etiologic import. Levi and de Rothschild 1 have called 
attention to the association of Basedow symptoms in this affection, and per 
contra the total absence of myxedema in any of the reported cases. Thus, 
they believe a thyroid dyscrasia is a factor in the production of the disease. 

Symptomatology. —We may divide the clinical course into three stages: 
firstly that of vasomotor symptoms ; secondly, that of marked trophic disorders, 
and thirdly; the period in which gangrenous sloughs or necroses are detached, 
local healing usually taking place with the subsidence of symptoms. 

The Stage of Vasomotor Phenomena. —Here belong the characteristic local 
syncope and asphyxia. 

Local syncope , when it affects a peripheral part, is characterized by 
sudden blanching and coldness, of varying intensity from cadaveric white to 
combinations of color, shadings with greenish bluish and red. A reduction 
in temperature of the part, and sensory symptoms are associated. Pares- 
thesiae and pain that follow or sometimes precede the syncope are variously 
described. Numbness, formication, radiating aches often give way to intense 
pain, accompanied by the sensation of a local benumbed or dormant state. 
In other cases only paresthesiae are noted. More or less rigidity or clumsi¬ 
ness of the fingers, when these are affected, associated with cold perspiration 
complete the picture of this stage. 

The pallor has been described as waxy, tallowy and dull, being rarely 
absolutely white, though a yellowish tint is not uncommon. More frequently 
than this discoloration does the-numbness and blunting of the sense of touch 
strike the patient’s attention; for it interferes with delicate movements. 

Strange to say, while occasionally encountered at the extremes of life, 
local syncope is chiefly seen in the period of active sexual life. In a case of 
the author, as also in one recorded by Raynaud, the liability to local syncope 
always ceased during the early months of each pregnancy. 

Emotions, worry, exposure and fatigue seem to incite a fresh attack; other 
motivating agents being water, especially if cold, or even the handling of 
cold articles. In some cases it may occur at any hour without obvious 
reason. Monro speaks of the association of flushing of the face with pallor 
of the fingers. This may occasion great mental distress to the patient, 
especially when such changes occur at meal times and are conspicuous to 
others. 

Monro’s 2 tabulation of clinical data in 176 cases-, records 3 in which local 
syncope was alone observed; 20 in which it was associated but not always 
synchronously with local cyanosis; and 66 other cases in which necrotic and 
sclerotic processes were added to the local syncope—almost always, but not 
invariably after a stage of local cyanosis. On the other hand, there were 
28 cases in which local cyanosis alone was observed, and 56 other cases in 
which neurotic or sclerotic changes followed upon local cyanosis without any 
stage of local syncope being noted. 

The Local Asphyxia. —The color of the skin changes to a bluish, purplish, 
violaceous hue, or may haVe a blue-black tint admixed with red. The 
adjacent parts have marmorated appearance. Here, too, a fall of local 
temperature is to be expected. 

1 Levi et de Rothschild, La petite insuffisance thyroidienne, Paris, 1913. 

2 Monro, T. K., Raynaud’s Disease, Glasgow, 1899. 


RAYNAUD’S DISEASE 


547 


The usual distribution is over either the fingers, toes, tips of the nose, or 
ears. Pressure upon the affected part with the examining finger demonstrates 
how sluggish is the return of blood. 

A certain degree of swelling is rarely missed during this phase, whilst with 
the syncope, a slight contraction of volume is usual. The enlargement 
or puffiness is not due to edema, and may appear simultaneously with or 
precede the asphyxia. When it is extreme, which is rare, it should be regarded 
as of angioneurotic nature. 

The degree of fall of temperature may vary in the fingers. Most inter¬ 
esting is the observation of Hoesslin, 1 who found on actual measurements that 
the temperature of the asphyctic part may drop some 4 0 C. to below that 
of the air. 

A diversity of tinting has been reported ranging from typical asphyctic 
and livid hue to a fuchsin or crimson discoloration of areas that are sharply 
demarcated from their surroundings. Intense rubor may follow in the wake 
of the asphyxia, last for hours, thus mimicking erythromalalgia. This color, 
however, is never that of hyperemia, but rather of a rose or bright red. 

The syncope and asphyxia may occur simultaneously; certain phalanges 
may have a gray-blue or ashen gray and blue tint, adjoining other phalanges 
in which blanching can be observed. A play of colors with many shadings 
from cadaveric white into several tints of red, and the different asphyctic 
changes mentioned above, is not an uncommon phenomenon. 

As to the onset of asphyxia, the author’s observations lead him to believe 
that it may precede the syncope or the latter may be wholly absent. Cassirer, 
Weiss and others report asphyxia as signalizing the onset in many cases and 
mention that it may occasionally completely fail to appear. 

When both local syncope and asphyxia occur, the former is usually the 
earlier phenomenon; but in exceptional cases, where the reverse order obtains, 
cyanosis may yield to blanching with a disappearance of the latter after a 
few minutes and a return of the blueness. 

The asphyctic stage may last a few minutes, hours or days, may recur 
once or more often during the day or after intervals of days. On the whole, 
its duration is somewhat longer than that of syncope. 

As for situation, the acroterial localization is not as characteristic a 
feature of local asphyxia as of the syncope. It may be more conspicuous 
over the hands than over the fingers, or the latter may be free whilst more 
proximal parts are notably invaded. It may not be confined to the phalanges 
but may affect the hands and feet, or even the forearms and legs. Both 
cyanosis and syncope may occur coincidentally. For example, the distal 
portion of the fingers may be blanched whilst the remaining sections of the 
hands are livid. 

Trophic Disorders and Gangrene.—Usually a small bleb with sero-san- 
guineous or blackish content develops at the tip of one of the fingers. When 
this opens, small erosion or ulcer remains for a variable length of time, till it 
cicatrizes. Or there is dry dystrophic process in which a dark scab forms and 
subsequently becomes detached in a scale-like manner. Another type of 
trophic change begins as a sort of induration and thickening at the finger tip, 
with consequent detachment of scaly epidermal masses; or larger blebs 
may burst, giving way to blackish necrosis of the skin on the separation of 
which deeper ulcers are disclosed. Although a dry gangrenous process is the 
rule, wet gangrene my occasionally develop. 


1 Hoesslin, Miinchen. med. Wchnschr., 1910, p.29. 


548 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


We expect to find symmetrically situated peripheral parts involved (fingers, 
toes, ears, nose) over limited areas. Occasionally, however, such symmetry 
is missed, and the affection has been known to implicate the sternal and buccal 
regions. In very rare instances large portions of a limb have become 
gangrenous. 

Monro’s 1 statistics regarding the relative frequency of gangrene in various 
situations are: In 43 per cent the upper; in 24 per cent only the lower; and in 
22 per cent both upper and lower extremities. 



Fig. 167.-—Disappearance of the termial phalanges in an case of a sclerodactyly and 

Raynaud’s disease. 

ThejOsseous Changes.—Characteristic changes are demonstrable in 
certain of the bones by X-ray examination. In the hand, the marked bony 
atrophy with the disappearance of one, more, or all of the tips of the first 
phalanges are the notable alterations of diagnostic value. Trophic bony 
changes involving not only the tips of the end phalanges, but reported as 
extending as an atrophic process as far as the metacarpus, with the possi- 

1 Monro, T. K., Loc. cit. 


RAYNAUD’S DISEASE 


549 


bility of restitution after recovery, are almost pathognomonic lesions (Figs. 
167 and 168). 

Sensory symptoms according to Raynaud are striking features of the 
symptom-complex, attaining considerable intensity during the stage of 
asphyxia, and abating with the period of reaction when paresthesiae appear. 
Some writers minimize the role of pain, whilst Cassirer and the author are 
inclined to subscribe to Raynaud’s views. 



Fig. 168.—Changes in the terminal phalanges in Raynaud’s disease. 


The pain may initiate the attack or may come on during the asphyctic 
stage; it may begin with severity or attain the maximum gradually, the degree 
being occasionally so great as to warrant injections of morphine. The pain 
has this in common with that of erythromelalgia and the acroparesthesia, 
that it is not confined to the distribution of single nerves, but is diffused 
over the affected extremity in regions roughly corresponding in extent to that 
of the vasomotor and trophic disturbances. In many cases investigated 
in this regard, no accurate localization of the sensory, irritative and the 
deficiency symptom could be determined. The pain was always of a different 


550 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


type than that of neuritis. Indeed, the belief has been expressed that the 
character of the pain and its close relationship to the vasomotor phenomena 
warrant the conclusion that v as o sensory fibers may be involved; and that these 
may be irritated either in the periphery or from some central point. 

Regarding the objective sensory disturbances these, too, are not limited to 
any particular nerve. In many cases they are absent. When present, 
hypesthesia or anesthesia are the most common, although most remarkable 
varieties and combinations have been reported: thus anesthesia of parts 
affected by syncope, with no sensory alterations in the free intervals; tactile 
changes and hypesthesia of all varieties over the whole hand, hypalgesia and 
thermohypesthesia. 

As for the motor disturbances, paralyses are not observed except in 
exceptional instances where muscular atrophy follows, and in which the 
interossei and muscles of the thumb participate. 

Remote Clinical Phenomena. —Occasionally there are interesting mani¬ 
festations of manifold types in territories quite remote from the peripheral 
parts heretofore described as implicated. It has been recently observed 1 that 
fall in blood pressure, diminution in the number of leucocytes, and accelera¬ 
tion of the blood clotting time occur during the attacks in Raynaud’s disease. 
The left cervical sympathetic nerve was affected in a case of Weiss, the left 
cheek becoming suddenly warm and red, associated with retraction of the 
left eyeball, hyperhidrosis and contraction of the pupil. A recession of all 
manifestations except for slight retraction of the eyeball was complete within 
a week, but recurrences took place, until finally a sort of partial atrophy 
of the soft parts of the left side of the face remained . 

Arthropathies with effusions into the joints of the fingers and knees; 
transitory disturbances of speech; cardiac palpitation, contraction of the 
retinal arteries are mentioned amongst the remote symptoms. 

Arterial Pulsation. —The radial artery is said by some authors to become 
pulseless during the stage of syncope, and this circumstance has been 
attributed to the arterial spasm. As a rule, however, the arterial beats can 
be elicited even though a diminution of force and some acceleration occur. 
Westphal has described, and erroneously grouped under the designation 
“Intermittent Claudication,” a case in which the pedal pulses disappeared 
during an attack. 

Other Evidences of Vasomotor Instability. —Amongst the many signs of 
vasomotor lability and neuroses associated with Raynaud’s disease are the 
following: A neurotic temperament with tendencies to emotional outbursts; 
attacks of migraine and polyuria with or without symptoms of hyperthyroid¬ 
ism; transitory or fugitive edema and urticaria; a marmorated skin; the 
associated complex “epidermolysis bullosa hereditaria” (Linser 2 ) with its 
tendencies to bulla formation and gangrene of the skin upon exposure to 
cold; multiple small epidermal hemorrhages; hemoptysis and hematemesis: 
chorea; and epileptiform attacks. 

Demonstrable Phenomena. —Although the production of pallor on elevating 
the limb to the vertical is usually a distinctive feature of the obstructive 
diseases of the arteries, it can be occasionally evoked in the spastic vasomotor 
affections. In a case of Raynaud’s disease of the upper extremities 3 ischemia 
and even reactionary erythromelia were elicited during the paroxysms on 
several occasions. We cannot, therefore, except with certain reservations, 

1 Souques and Moreau, Bull, de l’Acad. de Med., 84, 1920, p. 44. 

2 Linser, Arch. f. Dermat. u. Syph., 1907, LXXXIV, p. 6. 

3 See p. 544, case R. S. 


RAYNAUD’S DISEASE 


551 


accept these artificially produced phenomena as absolutely pathognomonic 
for the obstructive types of arterial disease. There is this distinguishing 
feature, however, that these responses are demonstrable only during the par¬ 
oxysm in the vasomotor neuroses, and whilst they can be constantly evoked 
in the obstructive arterial affections, and even in the former, they occur 
only when a spastic condition in the larger veins does not impede the return. 
And so, when confronted with the early vasomotor stage of thrombo-angiitis 
obliterans with pulsation still present, and involvement of but restricted 
arterial territory, the development of a continuous phase of response to the 
gravity tests is pathognomonic; occasional ischemia on elevation during 
attacks of vasomotor spasm may lead to erroneous conclusions. In the 
Raynaud complex, then, the hyperexcitability for vasoconstrictor responses 
may be motivated, perhaps, by this minimal gravity depletion. 

Another interesting difference between the angiospastic and obstructive 
arterial affections is the circumstance that reactionary rubor or hyperemia 
can be produced in the neurotic types even in the vertically elevated position 
of the limb (after release of tourniquet). From this the conclusion can be 
drawn that whilst diffuse vasoconstriction may be present sufficient to mani¬ 
fest itself as slight ischemia on elevation, the hydrostatic factors can be over¬ 
come. Evidently the degree of functional impediment to the flow of blood is 
not too great in the larger channels. The arterioles and capillaries, too, are 
not in such a state of insurmountable tonic vasoconstriction that they are 
unable to respond after release of the tourniquet. When the same mechanical 
forces are brought into play in thrombo-angiitis obliterans, obstructive 
arteriosclerosis and other obliterative organic vascular lesions reactionary 
rubor is absent in the limb held up to the vertical. 

These and other noteworthy phenomena are well illustrated in the notes 
from the following case: 

On physical examination of R. S. (previously cited) both hands are found to be cold 
(examined under artificial light). The tips of the first, second, third and fourth fingers of 
the right hand are slightly cyanotic; the tip of the fifth finger red. Over the dorsal aspect of 
the second phalanges of the second, third and fourth fingers there looms up a patch of blanch¬ 
ing which rapidly disappears, giving way to a slightly scarlet hue. A similar play of colors 
occurs over the left hand where the swelling is less marked than on the right. The palms 
are fairly red, except for cyanosis of the tips of the fingers. The radials apparently are less 
tense than they were at the last examination. The heart is negative. 

On elevation of the hands, the cyanosis of both seems to diminish, practically disappear¬ 
ing in the right hand, yielding more slowly in the left. The patient says that elevation 
also improves the subjective state, inasmuch as the uncomfortable sensations of the fingers 
diminish; these seem less swollen, less rigid. 

On hanging down, after preliminary elevation, the whole hand is red except for slight 
mottling due to cyanotic patches near the tips. On applying a tourniquet after elevation of 
the right arm, the hand becomes distinctly cyanotic, except for the fingers, which exhibit 
only patches of lividity. On releasing the tourniquet in the elevated position, rapid and 
intense reactionary erythromelia is elicited; it involves the whole region distal to the site of 
constriction. The tips of the fingers are cyanotic, the deep flush disappearing within a 
minute, normal color returning in about 2 minutes. 

Scleroderma, Sclerodactyly and Raynaud’s Disease.— Raynaud phe¬ 
nomena not infrequently occur coincidentally with, preceding or following the 
development of the indurative and atrophic stages of scleroderma and sclero¬ 
dactyly. Indeed, because vasomotor disturbances are such early and 
common manifestations of scleroderma, a differentiation from the Raynaud 
complex has often been regarded as almost impossible. 

Local cyanosis or local numbness may antedate by years the character¬ 
istic symptoms. Particularly in sclerodactyly are vasomotor phenomena 
apt to occur as prodromal signs. These are the cases in which the clinical 


552 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


picture is that of Raynaud’s syndrome for a long time and in which mixed 
types then develop, the differential segregation of the two diseases being not 
feasible. Local asphyxia and local syncope have been known to dominate 
the clinical picture for a long period in advance of the sclerodermic condition. 

Since, in the course of Raynaud’s disease, besides the typical trophic 
changes of gangrene, certain chronic dystrophic processes may be associated 
such as lead to induration and thickening of the skin and subcutaneous tissue, 
it is little wonder that the similarity of the two affections can be very close. 
For the recognition of such intermediary types, Cassirer suggests the following 
grouping. 

1. Typical Raynaud’s Disease.—This includes cases in which in addition 
to the symmetrical gangrene, dystrophic alterations involve the distal parts 
with thickening of the skin and immobilization of the tendon sheaths and 
joints. The skin although smooth, tense, unyielding is not typical of sclero¬ 
derma; and furthermore its involvement is limited to those parts in which 
the vasomotor and trophic symptoms of Raynaud’s are most intensely 
represented. 

2. In this group we may gather the cases in which local asphyxia and 
syncope initiate the disease, with a long period of paroxysms. Instead of a 
further progression into the stage of gangrene, there is a chronic stage 
attended with abatement of the vasomotor and sensory manifestations and 
with the development of true sclerodermic phenomena—not only ov.er the 
acra, but even implicating the face, breast, arms and other parts. 

3. A third type is constituted by those relatively rare instances in which 
the vasomotor symptoms emerge in the midst of the completely elaborated 
picture of scleroderma. 

To these we may add cases described by the author, 1 in which a period 
of vasomotor phenomena precedes the objective signs of thrombo-angiitis 
obliterans, both the upper and lower extremities being the sites of attack. 
In a second period the symptoms of thrombo-angiitis obliterans with gan¬ 
grene are so well developed as to be easily recognizable, although in the case 
of the hands, alterations simulating sclerodactyly may finally come into 
evidence. Such patients suffer from true organic obliteration of the arteries, 
and simulate not only Raynaud’s disease but also sclerodactyly in part of 
their clinical course. 

The following differential schema has been suggested by Castellino and 
Cardi. 2 


Sclerodactyly 

Symmetrical affection of the hands. 
Progressive course. 

Color usually first red, less bluish. 

Skin cold, hard, swollen and congested. 
No sensory disturbances; feeling intact. 
No pain or paresthesiae. 

Frequent occurrence of “sclerodermic 
mask.” 

More frequently in children. 


Raynaud’s Disease 

Symmetrical affection of the hands. 
Interrupted, intermittent course. 

First whiteness, then blueness. 

Skin cold, congested, swollen, not very hard. 
Anesthesia. 

Severe pain and paresthesiae. 

No sclerodermic mask; if present, coexist¬ 
ence of two maladies. 

More often in adults. 


Pathology. —A study of the literature by Dehio 3 and Cassirer has con¬ 
vinced both authors that a comprehensive adequate and satisfactory 
investigation into the pathological anatomy of a typical case of Raynaud’s 

1 Buerger, Am. Jour, of Med. Sc., Feb., 1915, No. 2, CXLIX, p. 210. 

2 Castellino and Cardi, Morgagni, 1895, L P- 625. 

3 Dehio, Deutsch. Ztschr. f. Nervenh., 1893, IV, p. 1. 


RAYNAUD’S DISEASE 


553 


disease is nowhere to be found. Where negative findings are recorded, the 
examinations were so incomplete as to be inacceptable. The reported 
arterial alterations, on the other hand, could under no circumstances be 
held responsible for the disease. In the various descriptions of nerve changes 
there are so many inconsistencies, their occurrence so inconstant that here, 
too, we must be chary in accepting any causal relationship. 

It must be conceded that all the vasomotor neuroses, of which the 
Raynaud complex is a prominent example, have one feature in common, that 
the arteries and veins have suffered no organic alteration in their patency. 
The varying objective phenomena arising from vascular instability must be 
attributed, therefore, to some vice of innervation. We are justified in assum¬ 
ing that an irritative (possibly paralytic) process in the vasomotor system 
is responsible. According to Cassirer, “Certain parts of the nervous system 
(vasomotor and trophic centers and paths), particularly the vasoconstrictors, 
are in a condition of increased irritability, a status brought about by an 
abnormal congenital Anlage 1 (predisposition) whose existence is indicated 
by the presence of other signs of hereditary neurosis; or, a condition that 
may be acquired through repeated noxious influences, as frequent exposure 
to cold, rheumatic disease or bodily or psychic traumata; or, the irritability 
may be evoked through infections and intoxications or reflexly through 
disease of distant organs, vessels or nerves. So that although, in this way, 
a number of variations from the disease type are developed, the unity of 
the Raynaud complex is thereby not invalidated.” 

Diagnosis. —If the typical picture of the Raynaud complex be borne in 
mind, and the dignity of the phemomena be not underrated, the differential 
diagnosis should not be difficult. It is the atypical forms, only, which may 
present trying problems. 

Thus, the mere presence of the so-called doigt-mort , or attacks of blanched 
cadaveric fingers, does not warrant diagnosing Raynaud’s disease. On 
the other hand, the absence of single symptoms, even of gangrene, must not 
militate against such diagnosis. 

A. Differentiation from Other Vasomotor and Trophic Neuroses, i. 
Erythromelalgia. —Although some cases seem to have symptoms bordering 
on those of Raynaud’s, a clinical distinction may be made. In both, localiza¬ 
tion, symmetry and sudden onset may coincide. However, the rubor, dis¬ 
appearing on elevation, the attacks of pain, the normal or increased sensibility, 
the very slight trophic disorders, if any, the increased temperature of the 
part with a feeling of warmth, the normal reflexes, all these should speak for 
erythromelalgia. 

In Raynaud’s syndrome, the dark bluish, purplish or blackish discoloration 
(in second stage) uninfluenced 2 by elevation, areas of analgesia, diminished 
sensibility or anesthesia, the well marked trophic disturbances, the dimin¬ 
ished temperature and feeling of cold, the diminished reflexes (occasionally 
absent), and the rare motor phenomena (of paretic nature) are characteristic. 
However, that cases of Raynaud’s may occasionally present certain of the 
symptoms of erythromelalgia cannot be denied. 

2. The acroparaesthesice of Schultze 3 or Nothnagel form a clinical complex 
distinguished by the gradual or sudden onset of paresthesiae, a sensation of 
numbness or “dead feeling” as if the fingers were absent, occasionally formi¬ 
cation with tearing or dragging pains, and always attended with a sensation 

1 Not in the anatomical sense. 

2 Note that this may not obtain in certain atypical cases. 

3 Schultze, Deutsch. Ztschr. f. Nervenh., 1892, III, p. 300. 


554 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


of coldness. The fingers, hands, and arms are involved. The fingers become 
white, colder than normal, and the radial pulses are equal and always active 
even though the hands are unequally affected. Disturbances of tactile 
sense and a diminished sensibility for needle pricks, touch, temperature and 
electrical irritants exist. There is a symmetrical distribution which cannot 
be relegated to the territory of any particular nerve. Motor disturbances 
are absent. 

Schultze described a form without vasomotor symptoms (Schultze’s 
type), whilst Nothnagel one with sensory and vasomotor phenomena (Noth- 
nagel’s type). 

The differentiation of the acroparesthesiae with syncope from Raynaud’s 
may be difficult or impossible at times. Should cyanosis be superadded, 
even if only fugitive and occasional, the diagnosis of Raynaud’s disease 
would be permissible. 

3. Acroasphyxia chronica 1 manifests itself particularly as a gradually 
developing cyanosis of the end of the extremities, without paroxysms or 
attacks , associated with sensory or trophic disorders. In a second group 
marked trophic disorders appear, in that the soft parts are the seat of a 
chronic hypertrophy leading to pictures suggesting acromegaly. 

Although distinguished from Raynaud’s in its slow chronic progressive 
course, in the absence of attacks, and the permanent increase in volume of the 
affected parts, there are cases which seem to offer clinical transitions to 
Raynaud’s complex. Even in these, however, pain is insignificant, and 
syncope absent. The temperature is diminished, the cyanosis of the hand 
may extend to the middle of the forearm, although the palm is less affected. 
The enlargement does not involve the bones. 

4. Simple Vasomotor Circulatory Neuroses. —The incidence of a large 
variety of clinical symptom complexes, particularly in women, that mimic 
Raynaud’s disease, oft regarded as transitional stages in the development of 
the typical Raynaud complex, warrants a consideration and study of these 
conditions, so that the clinician may differentiate between maladies with or 
without gangrenous sequelae. From the standpoint of forecasting the future 
integrity of the limb in question, such diagnostic studies are of no mean 
importance, since the mild vasomotor neuroses are rarely associated with 
extensive trophic lesions. 

Their differentiation from the transitory circulatory disturbances occa¬ 
sionally accompanying organic occlusive lesions of the vessels is readily 
accomplished by noting the absence of the following signs in the vasomotor circula¬ 
tory neuroses: (1) Closed and pulseless vessels; (2) marked ischemia on 
elevation; (3) reactionary rubor; (4) erythromelia; and (5) chronic atrophic 
and dystrophic changes in the foot. Where the cases pass over into the 
Raynaud stage, the picture will change and the trophic and gangrenous 
phenomena can be expected. 

B. Differentiation from Organic Nerve Disease. —1. Atypical nerve affec¬ 
tions in which the diagnosis is doubtful are occasionally accompanied by 
Raynaud phenomena. Signs referable to organic nerve alterations should 
always tend to invalidate the diagnosis of a possible true Raynaud complex. 

2. Polyneuritis, as seen in beri-beri with irritative and paralytic mani¬ 
festations, may be exceedingly suggestive. Thus, loss of tactile sense, hyper- 
1 Crocq, Semaine med., 1896, XVI, p. 298. 

Kollants, Deutsch. Arch. f. klin. Med., LXXXVI, S. 504. 

Pehu, Nouvelle I Congr. d. I. Salpetr., 1903, p. 1. 

Barker and Sladen, Jour. Nerv. and Ment. Dis., 1907, p. 745. 

Cassirer, Die Vasomot. troph. Neurosen, Berlin, 1912, pp. 506-535. 


RA YNA UD'S DISEASE 


555 


esthesiae, absent knee reflexes with gangrene of the tips of the toes have been 
recorded in a case of beri-beri. Such an association of symptoms can in no 
wise be regarded as belonging to the Raynaud group. 

3. Syringomyelia. —It is the trophic disturbances in this affection that 
may lead to fallacies of interpretation. The slow development, the absence 
of symmetry, the pain and characteristic vasomotor symptoms should be the 
distinguishing marks of syringomyelia. Summarizing the different points, 
Castellino and Cardi 1 attribute to syringomyelia the following character¬ 
istics: An insidious onset, a slow course over many years (10 to 15), nutri¬ 
tional disturbances usually involving but one limb at the onset, recurring pain¬ 
less paronychiae, sensory disassociation, muscular atrophy, ulcer formation 
(perforating ulcer), loss of nails, ungual dystrophies, and necroses with 
sequestration of bone. Against these we find, in Raynaud’s complex, a 
sudden onset, rapid course, symmetrical appearance, dry gangrene, anesthesia, 
very little muscular atrophy, and bone atrophy. 

C. Differentiation from Vascular Disease. —The significant pathog¬ 
nomonic and distinctive feature of organic arterial disease is the obliteration 
of the usually palpable peripheral arteries. Gangrene due to cardiac and 
arterial disease (embolic and thrombotic gangrene), athero- or arteriosclerotic 
processes, and thrombo-angiitis obliterans (Buerger 2 ) should be recognized 
without difficulty. 3 

1. Thrombo-angiitis Obliterans. —When this affects the upper extremities 
it may be readily confused with Raynaud’s disease; for attendant true vaso¬ 
motor phenomena independent of the classical hydrostatic and mechanical 
signs, may be striking features. 

The symptoms simulating Raynaud’s disease and acroasphyxia are 
cyanosis of the finger tips, coldness of the fingers with or without trophic 
disturbance, and alternating cyanosis and rubor, involving the fingers or the 
whole hand. Rather characteristic in the symptomatology of thrombo¬ 
angiitis is the apparent dependency of the vasomotor symptoms upon 
variations in temperature, the chronicity of the manifestations, the absence 
of pain in some of the cases, and the absence of paroxysmal nature of the 
attacks so characteristic of Raynaud’s disease. 

Those patients in whom the trophic disturbances seem to be unassociated 
with evidence of vasoconstriction and vasodilatation give merely a history of 
the development of a spontaneous ulcer of the fingers. It seems more than 
likely that in many of these the history of the absence of the vasomotor pheno¬ 
mena would be found unreliable if it were possible to observe the cases through¬ 
out the whole course of the disease. 

Characteristic for thrombo-angiitis obliterans are the following groups of 
symptoms: (1) The disappearance of the pulses, particularly the dorsalis 
pedis, posterior tibial, and popliteal, more rarely the femoral, radial, and 
ulnar; (2) the development of typical manifestations of impaired circulation, 
to wit: blanching of the lower extremities when these are elevated above the 
horizontal, hyperemia (rubor) or reddening of the foot in the pendent position 
( a chronic condition which the author has termed erythromelia) during certain 
stages of the disease, and trophic disturbances, such as impaired growth of the 
toe nails, slightly atrophic condition of the skin, ulcers, and gangrene; (3) 

1 Castellino and Cardi, Morgagni, 1895, I, p. 625. 

2 Buerger, Jour. Med. Sc., Oct., 1908; Jour. Med. Sc., Jan., 1910; Surg., Gynec. and Obst. 
Nov., 1918; Med. Rec., Dec. 26, 1914; Jour. Med. Res.,'Nov., 1914, XXXI; Am. Jour. Med, 
Sc., Feb., 1915; Arch, of Diagnosis, Oct., 1915; Am. Jour. Med. Sc., Sept., 1917; New York 
Med. Jour., Mar. 13, 1920. 

3 For the application of Capillary Microscopy, see Chap. CVI et seq. 


556 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


true vasomotor phenomena of transitory nature, such as alternating syncope, 
rubor and coldness, apparently independent of these chronic changes that 
have been cited above and that are distinctly traceable to the occluded con¬ 
dition of the arteries and veins; (4) the symptoms of pain, either in the form 
of intermittent claudication (pain in the calf of the leg or in the foot on walk¬ 
ing with cessation when the limb is at rest) or the severe pain that is asso¬ 
ciated with the advent of trophic disturbances, especially with ulcers and 
patches of gangrene; (5) the slow course of the disease, symptoms of inter¬ 
mittent claudication or pain, preceding the development of trophic disturb¬ 
ances for months and years; (6) the fact that more than 95 per cent of the 
cases occur in Polish, Galician, or Russian Hebrews, and that amost always 
young males between the ages of 20 and 30 are affected with this disease; 
(7) the common onset of symptoms in the lower extremities, one of the legs 
being usually first affected; (8) the comparative infrequency of involvement 
of the upper extremities; (9) the association of a peculiar type of migrating 
phlebitis in the territory of the external or internal saphenous, less frequently 
in the larger veins of the upper extremities characteristic in about 20 per cent 
of the cases, and sometimes antedating the subjective and visually objective 
signs in the legs; (10) the slow but steadily progressive course, leading in a 
large majority of the cases to amputation of at least one limb, not infrequently 
of both lower extremities, and in rarer instances to amputation of one of the 
upper extremities as well. 

Even a rapid review of the salient symptoms of thrombo-angiitis obliterans 
would seem to suffice to leave the impression that it could hardly be mistaken 
for other diseases. And were it not for the fact that certain symptoms closely 
resembling typical vasomotor phenomena may persist for weeks and years in 
this disease, confusion with the true neurogenic vasomotor processes would 
scarcely ever arise. The chronic condition of redness in thrombo-angiitis 
obliterans can be explained as due to dilatation of the superficial capillaries, 
this being a compensatory phenomenon making for an adjustment of the 
impaired circulation. This chronic redness or rubor may be mistaken for 
erythromelalgia or for the rubor of Raynaud’s disease. The fact that it is 
associated with other evidences of closed vessels and the other charactertistic 
features above mentioned together with the circumstances that the redness 
disappears at once upon elevating the extremity, will make the recognition of 
its nature possible. 

In addition to this more or less chronic or permanent sign of deranged 
vasoconstriction, other phenomena which are truly vasomotor in nature may 
frequently be associated in thrombo-angiitis obliterans, and it is these that 
must be differentiated from similar phenomena accompanying Raynaud’s 
disease, erythromelalgia, scleroderma, sclerodactyly, and acrocyanosis. 

If we do not overestimate the importance of single manifestations of 
vasomotor irritation, but regard as more significant the clinical course and the 
symptoms in their totality, we will not fail to separate very clearly in our 
minds the true vasomotor phenomena. 

It is true that there are still some who cling tenaciously to the theory 
that some lesions of the peripheral arteries may account for the symptoms of 
Raynaud’s disease. In support of this view certain anatomical findings have 
been cited as strong arguments by those who believe that a definite anatom¬ 
ical lesion in the peripheral vessels is irresistible testimony against pure hypoth¬ 
esis. A careful analysis of the cases in question, as made by Cassirer, shows 
that reported organic alterations in the vessels will not suffice to explain the 
symptoms any more satisfactorily than the theory of a central nerve affection 


RAYNAUD’S DISEASE 


557 


of the sympathetic system. Whereas in thrombo-angiitis obliterans the 
territory manifesting symptoms corresponds to that containing the diseased 
vessels, we find that no such relation exists where vascular lesions are asso¬ 
ciated with Raynaud’s disease. 

For the clinical diagnosis of thrombo-angiitis we must depend upon (i) 
the racial (Hebrew) and sex (male) predilection; (2) the early involvement 
of the lower extremities; (3) the early symptoms of pain or intermittent 
claudication; (4) the presence of migrating phlebitis; (5) the evidences of 
pulseless vessels; (6) the presence of blanching of the extremity in the elevated 
position; (7) the existence of rubor in the dependent position; (8) the relation 
of the hyperemic phenomena to posture; (9) the absence of simultaneous, 
symmetrical involvement, and (10) the slow, progressive chronic course 
terminating in gangrene. 

Whereas in thrombo-angiitis obliterans a definite and specific morpho¬ 
logical change in the arteries and veins is responsible for the varied phenomena 
in the superficial capillaries, in Raynaud’s and allied diseases the vasomotor 
and trophic disturbances are the outcome of irritative and exhaustive processes 
of the sympathetic nervous system. 

Furthermore, characteristic for Raynaud’s is the osseous atrophy and the 
striking absorption and disappearance of the terminal phalanges, well demon¬ 
strated by Roentgen ray examination. 

2. From organic arterial diseases in general, the following differential signs 
characteristic of obliterated arteries should be sought for by a thorough 
clinical examination. When these can be elicited, Raynaud’s syndrome can 
be excluded. They are: 

(a) The symptoms of intermittent claudication, which is a clinical entity 
but accompanies occluded arteries of the lower or upper extremities from 
numerous causes. 

(b) Coldness of the extremity, particularly influenced by climatic 
conditions, occurring spontaneously or brought on by exertion. 

(c) Cyanosis or a bluish discoloration of the tips of the toes particularly 
the great toe, sometimes the ball of the foot, attended with coldness and 
particularly noticed after walking and in cold weather. 

(d) Ischemia or blanched condition. Whiteness or a blanched condition 
of the extremity, occurring when the limb is in the horizontal, rarely even in 
the dependent position, and which can be elicited on examination by elevating 
the affected limb 6o° to 90° above the horizontal (also known as ischemia). 

(e) Redness or rubor. A condition of redness or rubor, involving the toes, 
sometimes the dorsum and the plantar aspects of the foot for varying dis¬ 
tances to the ankle or even higher, frequently involving the lower extremities 
when these are allowed to hang down, occasionally occurring even in the 
horizontal position of the limb, and independent of infection, gangrene, or 
trophic disorder. The author has termed this phenomenon “ erythromelia. ” 

(/) Absence of pulsation. Absence of pulsation in the usually palpable 
vessels of the extremities, the dorsalis pedis, posterior tibial, popliteal or 
femoral of the lower extremity, the radial, ulnar and brachial arteries of the 
upper extremity. 

(g) Trophic disorders including indolent fissures, ulcers, hemorrhagic 
areas, superficial ulcers, perforating ulcers, a withered or atrophic condition 
of portions of the extremity, foot or hand, impaired growth of nails, etc. 

(h) Thrombosis. Attacks of thrombosis with the following symptoms 
referable to the sudden closure of vessels: Pain in the calf of the leg or in the 
foot, inability to walk, coldness, blanching of the foot on elevation, loss of 


558 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


pulsation in the dorsalis pedis, posterior tibial or popliteal arteries, or all of 
these, sometimes followed by development of trophic disturbances, and 
even gangrene, or at other times eventuating in more or less complete 
recovery. 

Treatment. —Unfortunately we have very little to offer in the way of 
therapy in this disease, since our knowledge of the etiology and pathogenesis 
is so meager. Our first care should be towards the attainment of improve¬ 
ment in the neuropathic diathesis, according to the well established rules 
laid down in Chap. CV. 

Monro points out that since the vasomotor centers have the tendency to 
act with abnormal readiness in this malady, measures should be adopted to 
avoid everything that favors the occurrence of the individul paroxysms; and 
that the patient should learn to escape the conditions predisposing to an 
attack. Thus every precaution should be taken to avoid under exposure. 

Not only should the feet be well clothed at all times, but gloves should be 
worn without causing the slightest interference with the circulation of the 
hands. In the worst cases it may be expedient for the afflicted to remain 
indoors in cold weather, with the room temperature kept warm at all times. 

The application of electricity has been much vaunted as of exceptional 
value. Although a beneficial effect is occasionally obtainable, this measure 
has on the whole been found disappointing. Galvanic hand and foot baths 
of io minutes’ duration are recommended by some authors. 

One broad electrode as cathode is placed against the nape of the neck, 
the second, or anode, is placed in luke warm water in which one or both hands 
or feet are immersed. The current strength is regulated so that distinct 
prickling is experienced, the seances lasting at least io minutes. Both pain 
and vasomotor symptoms may be beneficially influenced by such application. 

Good results are reported with the method of stasis or hyperemia sug¬ 
gested by Cushing, and applied by means of an elastic bandage. An ordi¬ 
nary muslin “ideal ” (semielastic woven bandage) or rubber bandage is made to 
compress the upper arm until distinct venous stasis ensues, without, however, 
interfering with the arterial supply. A good result can often be observed, 
although occasionally the pain is intensified. 

For the pain, rest with elevation of the affected parts and the usual coal- 
tar sedatives may be tried. Pyramidon, even more than antipyrin and 
phenacetin, seems to enjoy a favorable reputation. At times one will have 
to resort to morphine, although opium in other forms should be given a 
prior trial. 

Little is to be expected of the vasodilating remedies. Both amyl nitrite 
and nitroglycerine have been found wanting, although beneficial in certain 
cases. Pilocarpine is believed by Hoesslin 1 to give temporary relief. 

Arsenic perhaps is the best internal medication at our disposal, adminis¬ 
tered per os in the form of Fowlers’ solution, or as sodium cacodylate 
hypodermatically. Papaverin recommended by Pal subcutaneously or intra¬ 
venously as a vasoparalytic agent may be given a trial. Papaverin hydro- 
chlorid is non-toxic, and may be administered in 0.03 to 0.08 gm. doses 
per os or subcutaneously, or 0.01 to 0.02 gm. intravenously. 

Thyroid extract has been recommended by some; adrenal extract bv 
others. 

In a case of Raynaud complex attributable to pituitary disease, the 
administration of this gland was followed by considerable improvement in 


1 Hoesslin, Miinchen. med. Wchnschr., 1910, 29. 


SCLERODERMA 


559 


the symptoms. 1 It is, therefore, important to establish whether an endo¬ 
crine deficiency is present in any given case, and to administer the corre¬ 
sponding endocrine abstract. 

The operation of periarterial sympathectomy or arterial decortication 
is recommended by some of the French authors (Leriche 2 ). Its value in 
this disease, however, has not as yet been satisfactorily demonstrated. 


CHAPTER C 

SCLERODERMA 

It is because of the almost imperceptible gradations from one type to 
another occasionally presented by the obstructive and vasomotor clinical 
syndromes—morbid processes of wholly diverse pathogenesis—that it 
becomes necessary for the student of the circulatory disturbance of the 
extremities to include in the scope of his differential investigations a knowl¬ 
edge of the disease known as “ Scleroderma.” Whilst indurative tegumental 
disorders are par excellence the manifestations of this disease, almost identical 
objective alterations are seen in the Raynaud complex and are occasionally 
associated with thrombo-angiitis obliterans. 

Mention has already been made in the chapter on thrombo-angiitis 
obliterans of the cases with marked sclerodermal changes in the upper extremi¬ 
ties, and how the dorsum of the feet and lower part of the legs not infre¬ 
quently show extensive indurative thickenings. But it is Raynaud’s disease 
with its not uncommon coexistent signs of hardening of the integument that 
has most often been brought into association with sclerodactyly. 

Most important of all, however, for differential diagnosis is the circum¬ 
stance that vasomotor symptoms, such as local cyanosis, may precede by 
months or years the fully developed and characteristic picture of sclero¬ 
dactyly. These are the striking clinical facts that warrant an examination 
into the salient features of this interesting malady in a work apparently 
devoted to another theme. 

The literature abounds with appellations descriptive of the cutaneous 
scleroses—also known as dermatoscleroses. Most of these clinical complexes 
are now regarded as having a similar pathogenesis. Except for the condition 
sclerema neonatorum (sclerema of the newborn) the oft separately classified 
affection of scleroderma , chronic progressive scleroderma, localized dermatosclero- 
sis, morphoea and sclerodactyly are best grouped under one inclusive term, 
namely, scleroderma. Since sclerema neonatorum is still regarded by a fairly 
large number of authors as being a distinct entity, attention will be focused 
on the other forms of dermatosclerosis which have certain features in common 
and which vary only in combinations of symptoms and their appearance. 

The following forms have been described: first, a circumscribed form or 
morphoea; second, a chronic progressive form or scleroderma; and third, a 
subordinate form of the latter termed sclerodactyly. 

Other descriptive appellations, such as scleroderma diffusa snd those 
describing the limited forms, namely, scleroderma en plaques and en bandes , 
are found in the French literature. 

1 Pribram, Munchen. med. Wchnschr., 1920, 67, 1284. 

2 Leriche, Soc. med. des Hopitaux de Lyon, Dec. 2,1919; Lyon m6d., Jan. 10, 1920, 40. 



560 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Symptomatology. —The cutaneous alterations have been divided into 
those of the first, or edematous stage; second, the indurative stage; and third, 
the atrophic stage. 

First, in the edematous stage the skin presents a hard edema, with a 
smooth cutaneous surface. This change may be localized to small areas, 
may be transitory, coming and going, or continuously present. Sometimes 
it is of patchy nature or diffuse, or it may involve a whole extremity. It may 
be limited to one or another toe, to part of the lower extremity, to the hand, 
or even the eyelids. Gangrene of a toe is said to have followed this edema. 1 

In the second, or indurative stage of the disease, the skin becomes hard, 
tense and stretched, often bound down, glistening, sometimes having almost 
a varnished appearance. By virtue of this change, the consistency of the 
skin becomes progressively harder, almost cartilaginous, board-like, and 
sometimes described as being even stony hard. It has been reported as 
encasing the body (en cuirasse). When the face is involved, it gives a typical 
mask-like appearance. 

While at first there seems to be thickening, in a consequent stage attenua¬ 
tion may take place, so that the integument is thinner than normal. In this 
way depressions are produced. In both of the two latter periods of altera¬ 
tion, the skin is bound down, and cannot be displaced. 

The areas involved may begin as small spots, or areas of pigmentation. 
Such have been described as having a reddish center, surrounded by a 
brownish red ring, the whole becoming indurated and prominent. Patches 
of whitish or violet color have been described. 

The disease may begin acutely, within a few days or weeks, developing 
rapidly in intensity and extent, or it may take a slow course, in which case 
manifestations take years to become well marked. 

The varied phenomena described by many authors as modifying the 
picture of scleroderma may be grouped under the following heads: first, 
disturbances in pigmentation; second, secretory changes; third, deranged 
vasomotility; fourth, trophic disorders; fifth, sensory disturbances; and 
sixth, disturbed motility. 

First, the pigmentation. Lewin-Heller 2 in their study of the literature 
report a brownish or yellowish white color change to be most frequently 
observed. A grayish color, too, is not uncommon. Such pigmentation is 
found in the form of stripes or patches, or may be diffuse in the sclerodermal 
as well as in other parts of the skin. Even the mucous membrane may show 
pigmentation. In some cases a combination of Addison’s disease and sclero¬ 
derma has been observed. An absence of pigment has been described. 

Second , the secretory changes. Either a general hyperhidrosis or increased 
sweating in the neighborhood of the sclerodermal skin is often a feature. 
But more frequently the affected parts show absent or diminished secretion 
of sweat. Probably the differences in reports depend upon the stage of the 
disease in which secretory activities were studied. Nerve influences are 
not unimportant in the determination of the activity of sweat secretion. 

Notes regarding the activity of the sebaceous glands have been made by 
some authors, and the glistening shiny appearance of the skin in some cases 
is regarded as an evidence of undisturbed or even overactive sebaceous gland 
cells. The opposite effects, however, follow necessarily when through atrophy 
the glands are implicated, and their activity ceases. 

x Legroux, Gaz. d. hop., 1880, p. 703. 

2 Lewin-Heller, Die Sklerodermie, Berlin, 1895. 


SCLERODERMA 


561 


Third , vasomotor disturbances. Local asphyxia or local syncope may be 
present for months or years before the symptoms of scleroderma manifest 
themselves. In the chapter on Raynaud’s disease we have referred to the 
cases of sclerodactyly—a form of scleroderma—in which the vasomotor 
symptoms are prodromal manifestations. Later, because of the combination 
of symptoms of scleroderma and disturbed vasomotor innervation, the diagno¬ 
sis may be difficult. 

Many authors, however, have called attention to cases of true scleroderma 
in which there was a previous history of excessive reaction to cold in the 
form of asphyxia or local syncope. Indeed, in one case a cyanotic discolora¬ 
tion and swelling of the fingers (Thibierge 1 ) existed for 7 years. 

In contradistinction to the asphyxia and syncope, other cases are reported 
as manifesting an active hyperemia, or such rubor associated with sensory 
symptoms. Thus, when rubor or painful paresthesia exists, a symptom- 
complex of the erythromelalgia type is present. The rubor may be diffuse, 
or appear in isolated patches; when of the latter type, it is particularly prone 
to be located near the joints. 

The so-called lilac ring that is said to surround the patchy scleroderma 
(morphoea) has also been explained as being of vasomotor origin. 

Regarding excessive response of the skin to external stimuli (dermato- 
graphism 2 ) Cassirer does not agree with other authors, who in describing 
the occurrence of urticaria in this disease would also emphasize an increased 
vasomotor cutaneous irritability. 

Possibly as manifestation of the disturbed vasomotor mechanism may be 
recorded the reduction of temperature of the part. Such obtains during 
attacks of syncope and cyanosis, but not in those of rubor. So, too, lowered 
temperature is noticed in the stage of atrophy. 

Fourth , the trophic disturbances. In addition to the characteristic skin 
alterations above described, we may mention the following: trophic ulcers, 
nutritive changes in the skin, such as marked desquamation and hemorrhages; 
or, of the adnexa of the skin in the form of alterations in the hair growth and 
changes in the nails. 

Of importance in differential diagnosis is the observation that ulcers 
occur especially at those bony prominences over which* the skin is already 
sclerodermatic or atrophied. They may, however, have a precocious develop¬ 
ment and appear in places that are not as yet subject to the specific altera¬ 
tions. Indeed, they may precede by months or years the advent of the 
typical phenomenon. Hardy 3 describes the occurrence of pustules or vesicles 
leading to the formation of superficial ulcers, then healing and the formation 
of superficial scars. Or, there may be very deep-seated ulcers destroying 
the skin and deeper tissue, and even with gangrene of small areas or territories. 

Indeed, gangrene has been frequently reported as complicating cases of 
scleroderma. Foulerton 4 observed a gangrenous patch on the dorsum of the 
foot, another over the internal condyle of one of the legs necessitating amputa¬ 
tion. Cassirer reports a case of painful gangrenous ulcer of a finger with 
sequestration of a piece of bone. He believes that ulcers may occur spon¬ 
taneously without previous vesicle formation, in that there develops a crust 
confining purulent fluid. The formation of ulcers is regularly attended with 
pain. Sometimes the ulcers are symmetrically situated. 

1 Thibierge, Soc. d. Dermat. et Syph., 1905, XII, 7. 

2 See chapter on Vasomotor Innervation of the Skin. 

3 Hardy, Gaz. d. hop., 1877; also 1881, p. 97. 

4 Foulerton, Lancet, 1892, XI, 12. 


36 


562 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


The disorders in the adnexa of the skin are especially disturbed hair 
growth. Most marked in the sclerodermal areas, does the hair become friable, 
thin, dry, and often of a bristle-like appearance. Or, there may be complete 
loss of hair over the whole body, the alopecia sometimes antedating the 
sclerodermal symptoms. 

The nails may become furrowed, easily broken, deformed, hook-like or 
crooked, may show membranous covering, or there may be atrophic condi¬ 
tions with degeneration of the nails into tiny platelets that may wholly 
disappear. Even the teeth are said to fall out spontaneously and the gingival 
mucous membranes atrophy. 

Fifth, sensory disturbances. In contradistinction to the Raynaud com¬ 
plex, scleroderma may be unattended with subjective sensory disorders, and 
may run its course without any pain whatsoever. According to the statistics 
of Lewin-Heller all sensory changes were absent in a large number of the 
cases examined. Thus, Cassirer noticed the existence of paresthesiae, 
burning sensations, itching, a dull feeling of numbness, or a sensation as 
if the part were asleep, often in the prodromal stage. Or, with paresthesia 
there may be attendant pain of tearing, sticking or burning nature. Or, 
there may be a feeling of tension in the skin that calls the attention of the 
patient to the cutaneous alteration. The pain may last for years, and is 
usually diffuse, not localized within the distribution of any nerve. 

Another evidence of sensory disturbance is the excessive reaction to 
cold, which may be so intense that the patients are unable to touch a metallic 
object, even a door-knob, for fear of exciting painful sensations. The 
sensibility may remain intact. However for the most part the sensory 
disturbances are not constant, may be absent, and the subjective sensations 
are infrequent and usually not well marked. In most of the cases the local 
condition runs parallel with the sensory disturbances and explains these 
sufficiently. 

Sixth , disturbed motility. Varying degrees of impairment of motion depend 
upon the situation of the scleroderma, the degree of involvement of the skin, 
and the implication of the deeper parts, the muscles and joints. Most 
striking of all is the immobility produced in the face through the cutaneous 
changes with the resultant changes known as the sclerodermal mask. Not 
only is there a fixation of the facial muscles, but, when the pressure attains 
sufficient degree, difficulty in opening the mouth, deglutition and mastication 
may be the consequence. 

So also, the interphalangeal joints may suffer becoming restricted in their 
excursions, and even fixed. 

When the muscles are involved, it is not uncommon to find atrophy 
usually due to muscular inactivity. Because of the difficulty encountered 
in palpating through the indurated skin, it may be impossible to distinguish 
between lesions of disuse from atrophy due to compression of the vessels 
and nerves, or, from sclerosis of the muscles themselves. In sclerodactyly 
muscular changes occur very frequently. Myosclerosis with an indurative 
condition of the muscle fibers has been reported. 

Complicating Lesions. Osseous Changes. —These may be both of the 
atrophic and hypertrophic variety, although the former is the more common 
and characteristic. Atrophy is especially noteworthy in the cases of sclero¬ 
dactyly, in which shortening and rarification of the bones occur. Even 
without trophic disorders or ulcers or gangrene, a gradual and total resorp¬ 
tion of the terminal portion of the phalanges, or a whole phalanx may develop; 
or, with the process less advanced, a narrowing and shortening of single 


SCLERODERMA 


563 


phalanges is noteworthy. This atrophy is well demonstrated in the 
Roentgenogram. Some authors describe an atrophic process of the long 
bones, with diminution in size and shortening of the arm bones. 

A particular clinical picture designated as acromicria has been described 
in which diminution in the size of the terminal parts of the phalanges gives a 
remarkable appearance. Because of the disparity in the thickness of the 
base of the fingers and their terminal digits, a characteristic tapering is 
developed. 

The rarefaction of the spongy bones may involve those (shoulder-blade) 
that are covered by normal skin. The reticular osseous structure may appear 
inordinately well marked in the X-ray pictures but the meshes are widened. 
Even foci of bone absorption have been noted. 

The so-called hypertrophic processes in the bone are not true enlargements 
as a rule, but often represent ossified myositis, or merely osteophytes. 

The Joint Lesions. —It has been noticed that rheumatic or articular con¬ 
ditions precede the development of scleroderma. Dercum describes a form of 
rheumatism, due in his opinion to secondary changes of a sclerotic nature. 
Ankylosing arthritis, fixation of the tarsal joints, implication of the inter- 
phalangeal articulations, and conditions similar to arthritis deformans are 
cited in the literature. 

The Mucous Membrane. —The tongue is most frequently involved and 
immobility of the mucous membrane as also atrophy, ischemia, participation 
of the pharyngeal and gingival mucous membranes are amongst the various 
lesions seen in this region. 

General Symptoms. —Most cases run a course without fever. Subacute 
febrile periods may develop with general malaise, insomnia, loss of appetite 
and diffuse pain. Blood examinations give varying findings, diminished red 
blood cells, increased eosinophiles or normal findings. There are frequently 
digestive diturbances, vomiting, constipation, sometimes diarrhoea, and 
nausea. 

Albuminuria occurs frequently, glycosuria occasionally. 

An important associated symptom is the enlargement of the thyroid 
occasionally seen, and sometimes sufficient to be regarded as Basedow. 

Vasomotor symptoms may partake of the Raynaud or angiospastic type, 
and more rarely resemble the picture of erythromelalgia. In the chapter on 
Raynaud’s Disease the occurrence and coexistence of the symptoms of the 
latter with sclerodactyly have been discussed. 

The clinical complex in such cases -comprises sclerodermal changes in the 
extemities, occasional attacks of local syncope, later ulceration and even 
gangrene. 

But even in that form of sclerodermal affection known as sclerodactyly , 
vasomotor symptoms are apt to be prominent, consisting of local cyanosis, 
local anemia, and hyperemia. Or, there may be recognized special groups in 
which the vasomotor manifestations take the following form: firstly, in a 
manner indistinguishable from typical Raynaud’s disease; secondly, with an 
onset consisting of local asphyxia and syncope, but without any progressive 
development into the typical Raynaud’s complex, symmetrical gangrene being 
absent; and thirdly, with vasomotor symptoms following the sclerodermal 
changes. 1 

Symptoms of Erythromelalgia. —Some authors have reported an asso- 
ication of symptoms of the three affections, erythromelalgia, Raynaud’s 

1 (Chap. XCIX, Raynaud’s disease with sclerodactyly.) 


564 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


disease and scleroderma. Attacks of local asphyxia, patchy or diffuse sclero¬ 
derma of the hands and feet, gangrene and pain, and periods of vascular 
dilatation over the hands—these complete a picture in which the signs of 
erythromelalgia are in evidence. 

Clinical Course. —The phases characterizing the development of this 
disease have been variously described. Probably the most useful classifi¬ 
cation is that into (i) a neurotic or prodromal stage; (2) one of edema; and (3) 
that of induration and atrophy. Because the cutaneous alterations may 
advance with varying degree of rapidity in different types of cases, such 
distinctions are only valuable as descriptive of the stage in which the lesions 
are found. Indeed, it would be almost impossible to put a limit to the 
prodromal stage in which vasomotor symptoms with or without sensory 
disturbances may dominate the picture. 

Then again, the cases have been grouped into acute or chronic, with 
innumerable transitions. The condition may last for many years, some 
authors reporting a protracted course. According to Lewin-Heller, there are 
instances with a duration of from 15 to 48 years. 

The disease does not progress continuously. Long intervals of apparent 
arrest or localized cessation with appearance of new areas of cutaneous 
involvement elsewhere may occur. Improvement has been noted even to the 
restoration of typical sclerotic zones into almost normal skin. Indeed, even 
complete healing is possible. Pigmented areas may remain after regression 
of the symptoms. 

Acute scleroderma develops occasionally in children, with well marked 
cutaneous changes elaborated within a few days, or a very few months. A 
chronic stage may supervene. 

Pathogenesis. —Four theories have been advanced in explanation of the 
malady: (1) Malfunction of endocrine glands; (2) infectious agents; (3) 
vascular; and (4) neurotic factors. 

Thyroid Imbalance .—Some believe that a primary disease of the thyroid 
gland is responsible for the elaboration of a toxin that produces the character¬ 
istic cutaneous changes. Indeed, it has been noted that scleroderma and 
Basedow may be associated. There does not seem to be much foundation 
for such a theory. Furthermore, the association of the two affections is not 
found in the majority of cases. Others suggest that both scleroderma and 
thyroid malfunction in Basedow’s disease may depend upon or be due to 
disturbance of the central innervation of the vegetative nervous system, and 
that the latter produces the anomalous function of this gland. There does 
not seem to be enough data to warrant the assumption that thyroid disease 
is a primary cause of scleroderma. 

As for the relation of the thyroid to the scleroderma, some authors are 
of the opinion that the malfunction of this gland in Basedow is rather the 
result of disturbances of innervation in the vegetative system, than of primary 
origin. In view of this assumption, whenever scleroderma and Basedow are 
associated, they refer again to the nervous system as the primary cause of 
the affection. 

The theory of abnormalities of internal secretions has received some sup¬ 
port and even a so-called pluriglandular insufficiency has been reported as 
responsible. To group it with Raynaud’s and similar affections or with the 
lepra group is unwarranted. Insufficient evidence is at hand at the present 
time to permit us to seriously entertain such an hypothesis. The vascular 
theory has been put forth as an explanation on the basis that the terminal 
arteries or arterioles are diseased. Binkler describes a perimeso and endarteri- 


SCLERODERMA 


565 


tis chronica fibrosa, especially of the skin vessels. Even though it must be 
admitted that changes in the cutaneous vessels do occur, it would appear 
that these are rather attributable to a primary, more remote causal agent 
somewhere in the nervous system. 

To the enlargement of the pituitary gland (Pribram 1 ) a causal influence 
has been attributed. 

The nerve theory finds its adherents who designate variously the 
central nervous system, the peripheral, or the sympathetic, either in an 
anatomic or a functional sense, as the cause of the malady. Lewin-Heller 
interprets the symptoms of scleroderma as due to disease of the vasomotor and 
trophic centers and paths; and since the anatomic basis for such an assump¬ 
tion has not as yet been satisfactorily discovered, the disease has been 
regarded by him as a vasomotor trophic neurosis, or an angio-trophoneurosis. 

The vascular theory can be rejected for it has never been proven to be 
present in advance of the sclerodermal changes; nor are there parallel or 
analogous alterations following arterial disease due to other causes. Nor 
could we explain by the vascular theory, the intermittent course of the 
malady, nor the sensory disturbances and other trophic derangements that 
occur here. 

Rather important confirmatory evidence in favor of the neurogenic theory 
is the close relationship between scleroderma and Raynaud’s disease and 
other vasomotor trophic neuroses. Indeed, the asphyctic symptoms, and the 
local syncope not infrequently form a part of the symptom-complex in sclero¬ 
derma, these manifestations, as before noted, preceding sometimes for months 
or even years with the appearance of typical trophic symptoms. There¬ 
fore, these diseases are intimately related, and both would seem to have a 
neuropathic origin. 

As for the nature and the locality of the lesions of the nervous system , little 
except hypothesis can be offered. Perhaps there are multiple motivating 
factors. But, as far as we know today, gross changes in the nervous system 
have not been found to account for the symptom-complex of the malady. 
We know that destruction of the higher vasomotor centers, namely, those 
parts that control the trophic functions of the tissues, does not produce 
scleroderma. As evidence we have the cases of transverse lesions oi the 
spinal cord; and even in gliosis, where there is long continued irritation 
through the proliferation of the glia tissue, severe intense trophic changes are 
observed, but not of the scleroderma type. 

Cassirer assumes that there is some sort of irritation of the higher centers which the 
subordinate centers cannot inhibit or control, and that this stimulus is brought about by 
varied moments, infection, exogenic and endogenic intoxication, and reflexes. 


Diagnosis— This is usually simple as soon as the characteristic cutaneous 
changes are developed. The early stages of the disease, however, particularly 
when abnormal localization occurs, may give rise to some difficulty of recogni¬ 
tion. These are the patients in whom the mucous fnembrane, the sub¬ 
cutaneous tissues, the bones, muscles and joints seem to manifest the 

first alterations. . 

In some cases the onset can be mistaken for the acroparesthesia?, bo, too 
local asphyxia and syncope may precede the development of the typical 
picture, and we have elsewhere referred to the similarity between the Ray¬ 
naud and scleroderma complex. 

1 Pribram, Deutsch. med. Wchnschr., 1920, 46, 87. 


566 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


In the persistent edemas (after cold, erysipelas, etc.), the consequent 
induration of the skin is but slight in comparison to that found in scleroderma, 
and atrophy does not occur. We have elsewhere alluded to the indurated 
edema, associated with spinal cord lesions (myelitis). 1 

In a case reported by Thibierge and Boutelier 2 there was associated edema 
that gave a picture simulating scleroderma. 

For the cutaneous phenomena of dystrophic nature occasionally observed 
in thrombo-angiitis, the reader is referred to Chap. LIX. 

Idiopathic Atrophy of the Skin {Erythromelie 3 ).—Under this caption 
symptom-complexes have been described in which cutaneous atrophy is 
characteristic. 


Pick suggested the name “Erythromelie,” Buchwald “idiopathic diffuse atrophy/’ 
Herxheimer “acrodermatitis atrophicans chronica progressiva” and “dermatitis atrophicans 
maculosa.” 

The disease usually begins with the formation of red or bluish red patches suggesting an 
inflammatory erythema, stasis, or passive hyperemia. These become larger and confluent 
until a large area of the skin is involved. Soon, an abnormal flaccidity or relaxation of the 
skin develops, with folding of the superficial layers; and an appearance of crumpled tissue 
paper becomes characteristic. Wherever displaceable skin is normally present, as over the 
back of the hand, knee and elbows, this plication is particularly accentuated. The skin 
becomes dry, adipose tissue reduced and the hair falls out. The vessels shine through with 
abnormal prominence in network-like fashion. Usually the affection is symmetrical over 
the extremities, the extensor surfaces being more intensively involved. Sensory disturb¬ 
ances are absent or very slight, there being no objective derangements of sensation, although 
slight pain may be present. 

Some French authors describe the skin of the affected region as showing a curious picture 
of atrophy and infiltration of apparently inflammatory nature, with an admixture of red and 
blue color as the striking phenomenon. The terminal portions of the extremities seem to 
suffer the maximum alteration, especially where the integument is almost in contact with the 
bony planes (elbows, knuckles, etc.). The affection develops chronically and usually 
attacks men between the ages of 30 and 50. In short, it is a sort of premature cutaneous 
degeneration. 

Various theories have been proposed in explanation of the malady. Some regard it as 
an anomaly of development; others attribute it to vasomotor lesions; and others accept a 
fundamental endocrine dyscrasia. 


Prognosis. —Although the type known as scleroderma proper often shows 
a tendency to improvement or healing, sclerodactyly is less apt to take this 
course. A cure is most likely to occur in the acute cases, and in general, it is 
stated that the prognosis is better in children where almost 30 per cent are 
believed to lose their manifestations. Improvement is reported by Lewin- 
Heller in about 30 per cent. 

A lethal outcome is very rare; but in severe cases, a sort of cachexia has 
been observed. The localization of the process has a bearing on the physical 
state. Impairment of mastication may make feeding difficult; or restraint 
of respiration through implication of the chest wall is an eventuality to be 
feared. Such are complications that impair longevity. 

Therapy. We possess no drug that seems to specifically influence this 
malady. Where healing takes place, it cannot be attributed to the drugs 
given. Thyroid extract and thyroidin have received most recommendation. 
Their value is, however, rather doubtful; they certainly are not specific. 
Other internal secretions as that of the adrenal have failed. Salol and 
salicylic preparations have been suggested and regarded as of some value by 
certain authors. Various forms of electric therapy also, electrolysis, elec- 

1 See Trophic Lesions in Chap. LXXXIX. 

2 Jhibierge and Boutelier, Soc. Fr. de Dermat. et Syphiligraphie, 1920, 27. 

• ? , ote J ;hat the appellation Erythromelia , as used by the author is not to be confounded 
with the German “Erythromelie” (Pick) found in German literature. 


MULTIPLE NEUROTIC GANGRENE 


567 


trie baths, have been much vaunted by some authors. Massage is of some 
value in increasing the suppleness of the skin, and overcoming the atrophy 
of inactivity, as also are hydrotherapeutic measures. Hot air treatment also 
has found its adherents, injection of thiosinamin (50 per cent alcoholic solu¬ 
tion), or fibrolysin, none of which, however, seem to have met expectations. 
Improvement of the general health seems to do as much as any drug for the 
condition. 


CHAPTER Cl 

MULTIPLE NEUROTIC GANGRENE 

There are observations in the literature on the occurrence of multiple 
gangrenous lesions of the skin that are not attributable either to changes in 
the vascular system, to alterations in the general nutritive condition of the 
patient, or to bacterial invasion. In most of the cases there were stigmata 
of nerve disease. The cases vary considerably in detail, so that a typical 
picture cannot be described. 

The large number of names suggested is in keeping with the variability 
of the symptomatology. They are acute multiple gangrene of the skin 
(Dinkier, 1 Zieler 2 ); multiple trophoneurotic gangrene (Muller 3 ); multiple 
neurotic skin gangrene (Kopp, 4 Joseph, 5 Adrian 6 ); also spontaneous skin gan¬ 
grene (Cronequist and B jerre 7 ); multiple insular necrosis of skin and subjacent 
tissue (Renshaw 8 ). 

In spite of the fact that many of the reported cases are artificial and 
occur in hysterical individuals, there remain some of undoubted authenticity, 
in these multiple neurotic, non-artificial gangrene occurs. Here belong the 
cases of Kopp, Hinter, Joseph, Doutrelepont, Singer, W. Sinkler, Neumann, 
Leloir, Renaut, Zieler, Kreibich and Bronson. 

Etiology. —Of twenty-five examples studied by Cassirer three were 
males; all were young individuals; eleven between the ages of twenty to 
twenty-seven; thirteen from eighteen to twenty years. 

Two factors, trauma and a neuropathic predisposition are seemingly 
essential for the production of the symptom-complex. In seventeen of the 
twenty-five cases, trauma is reported, and seven times a burn of the second 
degree. 

Such burns were noted seven times in a total of twenty-five cases. It 
would seem that through some agencies hypersensitiveness of nerves is 
brought about. That the history of previous burns is not merely coinciden¬ 
tal is attested by the large percentage of previous mechanical and thermic 
insults. Furthermore the intimate relationship between the locality of the 
gangrene and the previous injury is noteworthy. Often the site of necroses 

1 Dinkier, Arch. f. Dermat. u. Syphil., Bd. LXXI, S. 61. 

2 Zieler, Deutsch. Ztschrft. f. Nervenh., XXVIII, S. 184. 

3 Muller, Centralbl. f. inn. Med., Wiesbaden, 1902, S. 521. 

4 Kopp, Miinchen. med. Wchnschr., 1886, S. 665. 

5 Joseph, Arch. f. Dermat. u. Syphil., XXXI, S. 323. 

e Adrian, Deutsch. med. Wchnschr., 1902, S. 143* 

7 Cronequist and Bjerre, Arch. f. Dermat. u. Syphil., CIII, 0.103. 

8 Renshaw, Brit. Med. Jour., 1894, I, p. 1238. 


568 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


is confined to the side of the injury. In some cases the gangrene appeared 
a few days after the trauma, in others four to six weeks, and in still others 
many months or more than a year, in which case there could hardly be 
any relationship between the two. 

In a large percentage of the patients a diagnosis of hysteria could be made. 
In others the symptoms of general neurosis were present. However, the 
material at hand is not adequate to warrant the view that multiple gangrene 
is always a hysterical affection, although in the majority of instances neurotic 
stigmata are present. Multiple gangrenous foci have been observed in the 
territory in which motor and sensory disturbances of spinal gliosis occurred. 
In peripheral neuritis, other authors (Neuberger 1 ) report gangrenous areas 
of the skin. 

Where the lesions resemble a toxic urticaria, one would have reason to 
doubt the validity of the neurogenic theory of causation. Many of the other 
cases, however, because of the presence of a marked neuropathic diathesis 
and hysterical habitus, suggest a correlation between the two conditions. 
However, since this form of gangrene accompanies but very few instances of 
hysteria, the latter must be regarded rather as a predisposing factor than a 
causal one. 

An attempt has been made to explain the influence of the previous 
trauma as a causal factor. Wherever injury was noted, it would seem that a 
prolonged irritation on the peripheral nerve ending was present. • Such 
stimuli warrant the assumption that an increased irritability of distant 
vasomotor paths was thereby produced in a reflex fashion—in territories 
already labile by reason of the neuropathic disposition. 

Organic changes in the nervous system were not found in the one case 
in which an autopsy was performed. 

Symptomatology. —The most characteristic symptom is the appearance 
of multiple small necrotic areas in the skin without any alteration in the 
general condition to account for these, without any local bacterial infection, 
and without vascular lesions. 

Preceding the appearance of gangrene, burning and pricking sensations 
are experienced in the corresponding skin areas. Sometimes these sensations 
occur as prodromal signs preceding the latter by a few minutes, hours, or 
days. Or, an anesthetic sensation or itching and even pain in the vertebral 
region at the level of the lesion may antedate the onset. 

The sensory or irritative symptoms are not constant, and do not always 
accompany the advent of all of the necroses in any given case. At times the 
pains are very severe, or there are diffuse aches in the affected limb. 

Vasomotor symptoms are rare. In one case there was a large patch of 
urticaria, which became hyperemic, then hemorrhagic and finally showed a 
black spot in its center. This spot became gradually larger to about 3 mm. 
in diameter, and after twelve days began to sequestrate. The other necroses 
were of larger dimension. In the case reported by Truffi 2 severe pain was 
followed by pallor in the skin, with the development of an edematous glisten¬ 
ing area surrounded by a red zone. 

Some cases are reported as being preceded by the formation of blebs. 
According to Leloir formication is followed by the appearance of a red spot 
of varying size in the skin. After some hours a greyish white patch with a 
red surrounding zone develops in its center. After several hours there is a 
central depressed area that becomes yellowish, then darker until finally it is 

!? eu £ er I er ’ ^eutsch. med. Wchnschr., Nov. 20, 1902, Vereinsbeilag., p. 28, 1903. 

2 Truffi, Rev. de med., 1904, p. 992. ^ 


MULTIPLE NEUROTIC GANGRENE 


569 


blackish and gangrenous, the total duration of the process being from thirty 
to forty-eight hours. Doutrelepont 1 observed first hemorrhagic redness 
attended with burning and prickling followed by the formation of a yellowish 
spot. Other authors speak of the origin of gangrene in coalescing vesicles. 

The result of the various lesions described by numerous authors is a 
slough of varying appearance. It has been described as yellowish white, 
grayish, greenish gray, sometimes soft, other times dry and hard, and parch¬ 
ment-like. The size of the affected area is also variable (1X4 cm.), asso¬ 
ciated with spots the size of a lentil, 3 mm. in diameter up to the size of a 
dollar, or even larger. The necrotic area may be so hard that it cannot be 
penetrated with a pin or needle. Later an inflammatory zone usually 
appears about the slough. The defect after separation is usually super¬ 
ficial, rarely involving the subcutis. In one case, however, the mortifica¬ 
tion reached as far as the musculature (Hintner). The time required for 
the separation of the sloughs varies, the cicatrizing process being a slow 
one, taking from days to weeks and even months (4-5 months). Keloid for¬ 
mation is frequent. 

The mucous membranes, too may show lesions, though rarely. Necrosis 
in the throat, genitals, conjunctiva, mouth and tongue are reported. In 
one case there was first a vesicular eruption of the lower lip, and two months 
later a gangrenous vesicle in the territory supplied by the left trigeminal nerve. 
Two years later a gangrenous patch appeared in the neck, then over the 
upper arm, breast, upper lip and auditory canal. 

Clinical Course.— A nervous patient gives a previous history of trauma, 
after which either in the original scar, or in its vicinity, the first gangrenous 
patch appears. When the lesions are multiple, the youngest lesions are 
usually found proximal to the original one, so that various stages in the 
process can be recognized from above downward or from the center towards 
the periphery. The process may be limited to one side of the body, or after 
months may involve the other side. The cases of Truffi and Kreibich are 
typical, where both sides were involved but not synchronously. 

In the severe cases the lesions may be disseminated over the whole body 
Even the external auditory meatus and the ear-drum may be affected. 

The necroses may occur in rapid sequence and over considerable periods 
of time (3 years), during which there may be an almost continuous reappearance 
of necrotic areas. In one case (Sinkler 2 ) this period was 7 years, during the 
first 4 of which the left arm was affected, and later the right forearm. In the 
case of Truffi, the duration was about 17 years. In some cases the inter- 
mittence may be greater from several months to years. Therefore, the course 
is not unlike that described by Kaposi in his herpes zoster gangraenosa hyster¬ 
icus, in which the duration was from 10-20 years, with free intervals of weeks 
and months. 

Prognosis. —This is favorable as to life expectancy. As for duration, 
however, a prolonged period may be expected, with constant reappearance 
of gangrenous plaques. 

Pathogenesis. —Multiple neurotic gangrene cannot be regarded as a dis¬ 
ease sui generis , but rather as a symptom-complex. In most of the cases 
it would appear that changes in the nervous system could be held responsible 
for the necroses. There may, however, be a form of multiple gangrene due 
to multiple arteriosclerotic disease of the skin vessels (Cassirer). Even the 


1 Doutrelepont, Arch. f. Dermat. u. Syph., 1886, S. 179. 

2 Sinkler, Jour. Nerv. and Ment. Dis., 1897, p. n. 


570 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


true neurogenic forms are not of uniform nature. The process may be a rare 
symptom of organic nerve disease, such as spinal gliosis, tabes, peripheral 
neuritis and herpes zoster. Where necrosis is associated, we may speak of 
the lesion as urticaria gangraenosa. There is a marked hysterical habitus 
present in other cases. 

Diagnosis. —It is important in establishing a diagnosis to exclude the cases 
of malingering and artificial hysterical traumata. 

Thus, caustic soda has been known to have been employed artificially for the production 
of lesions by hysterical individuals. In the case of Striimpell, such was the case, but a 
marked dermatitis antedated the necrosis. Other caustics—such as zinc, chloride, sul¬ 
phuric acid, cantharides, hydrochloric acid, and crotin oil—have been similarly employed. 

As a differential point between artificial and spontaneous skin gangrene it 
has been suggested that in the spontaneous form, the necrotic, deeper portions 
of the skin can be seen through the superficial bleb. Furthermore, when the 
necroses appear in situations that are inaccessible to the manipulations of the 
patient, their spontaneous nature is thereby made apparent. Variability of 
the lesions, the polymorphic nature of the necroses, their irregularity in limi¬ 
tation—all these speak for artificial products. And furthermore, if they cease 
to appear, when the patient is under careful observation in the hospital, they 
are usually the result of malingering. 

The excision of pieces for microscopic examination (Zieler) has demonstrated that no 
destructive influences acting upon the surface can be noted. In the chemical necroses, the 
changes in the papillae are reactive in nature, and secondary to the external irritation, with 
very few or no changes in the deeper layers. 

It is well to search for organic nerve lesions in all cases, amongst these 
particularly spinal gliosis, tabes, and disease of the peripheral nerves. 

There is another form of multiple gangrene, which has no relation to the 
nervous system, but is an expression of a general cachexia. In addition to the 
latter symptom of asthenia, there are usually present the following manifes¬ 
tations: fever (which is absent in multiple neurotic gangrene), variability in 
the extent of the gangrene, and the rather restricted course, there being a more 
sudden development than in the multiple neurotic type. 

Therapy. —Arsenic, iron, calcium phosphate and potassium iodide have 
been recommended. Other authors have tried obstructive hyperemia with 
variable success. 


CHAPTER CII 

VASOMOTOR INSTABILITY 

There are a multitude of variations in clinical pictures offered by vaso¬ 
motor instability of the extremities. 1 The asphyctic symptoms may pre¬ 
dominate; or the pallor or signs of angiospasm or a tendency to simulate 
erythromelalgia may be a feature. Where the manifestations are associated 
with walking, a resemblance with the vasomotor type of intermittent 
claudication is striking. But, if we accept the warranted conclusion that the 
large majority of so-called cases of intermittent claudication are attended 
with organic disease of the vessels, usually obstructive, there remain those 

1 See also Chaps. CVII et seq. for recent work on the vasoneuroses and the vasoneu- 
rotic constitution. 


VASOMOTOR INSTABILITY 


571 


in which spinal cord vascular lesions are held responsible for the phenomena, 
and another type, in which true vasomotor symptoms seem to be evoked 
by muscular action. In some of the patients who make particular mention 
of the interdependence of symptoms and locomotion, close questioning 
demonstrates that such association is not at all essential, for symptoms 
may come on even when they are at rest. 

We should never lose sight of that group in which sensory and vasomotor 
derangements are attributable to thermic influences, whenever exposure to 
cold has been excessive, and was followed by chilblains or freezing of a part. 
It has been already pointed out that it is not uncommon for various phe¬ 
nomena of such nature to supervene months or even years after the part 
was subjected to cold. 

Vasoneurotic constitution is a term that has been applied to a condition 
characterized by instability of the vasomotor mechanism (Parrisius 1 ). Here 
alterations in vascular innervation manifest themselves either without 
apparent cause or after very slight provocation. Deviations in the caliber 
of capillaries occur over varied localities and in varying degrees at different 
times. Parrisius found that in the vasoneuroses the capillary loops at the 
base of the nails may evince remarkable differences in size, some being 
normal, others greatly dilated. 

In the pronounced cases of vasomotor lability, local arterial spasm may 
be a striking manifestation. The following is an example of vasomotor 
instability: 

Striking rubor in the horizontal position, occasional blanching of the big toe, 
occasional coldness and numbness on walking with pulsating vessels. 

T. H. W., 36 years of age, American, asserted that his feet and hands always had a 
tendency to become bluish and reddish during the winter months (Dec. 3, 1912). One 
month ago his left leg became somewhat numb, and gave him some trouble on walking. 
He thinks that 2 weeks ago his left leg was decidedly numb, and rather cold. For the last 
3 or 4 days the soles of the feet have been tender and there was pain in the left leg and thigh. 
Being a physician, he suspects that he has thrombo-angiitis obliterans. 

On examination, Dec. 3, 1912, the feet are distinctly colder than normal, and have a 
tendency to remain cyanotic. All the vessels pulsate strongly, the symptoms being more 
pronounced on the left side. The chief manifestations are coldness, and numbness of 
both feet, particularly the left. 

Diagnosis. Vasomotor neurosis. 

The patient was again seen on March 1,1915. Since he was last examined, he improved 
rapidly, and was almost free from symptoms until 6 months ago. At this time redness 
of both feet developed. This was particularly noticeable at night, and associated with 
some tenderness of the right foot. For the past 10 days the feet have been cold; both 
big toes have been markedly blanched. He stated that it required considerable rubbing 
to bring back the color. 

The Wassermann test was repeatedly negative, the blood pressure normal, migrating 
phlebitis and intermittent claudication absent. 

The chief symptoms, at the present time, therefore, are the numbness and coldness of the 
toes, the rubor at night and some weakness of the legs. 

Physical examination, March 2, 1915. In the horizontal position both feet are redder 
than normal, particularly the toes. The left foot is slightly colder than the right, but more 
than normal at the surrounding temperature. The color changes and the redness are 
accentuated through fluctuations during the period of observation. In the dependent 
position the redness does not deepen. In fact, the right foot loses some of its color, but the 
dorsum becomes more purple owing to the distension of the veins. There is no increase of 
the redness in the dependent position. On elevation a decrease of the rubor ensues. The 
upper extremities, too, are markedly red, but without symptoms. 

Conclusion. —A vasomotor case, the striking feature being the redness in the horizontal 
position, partly disappearing on elevation, but not completely: No true . erythromelalgia. 

In a communication received Sept. 25, 1922, the patient (a neurologist) says that the 
symptoms have completely disappeared, and he seems to regard them as having been of neu¬ 
rotic nature. 

1 For complete description of this complex see Chaps. CVII et seq. 


572 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Not infrequently the symptoms are attributed to exposure to cold 
although the influence of the latter cannot be accurately estimated. 

Vasomotor neurosis in a young woman , chronic rubor , and swelling of 
the hands. 

E. N., female aged 20 years, says her present condition has existed for nine years, was 
initiated by an attack of chilblains with both hands and toes frost-bitten. . Her hands are 
always red, somewhat swollen and moist, especially in cold weather, and neither electricity 
nor organotherapy have been of any avail. 

Physical examination (Dec. 23, 1919) revealed a somewhat nervous young woman, 
whose hands perspired profusely. The tips of her fingers were very cold, the whole of the 
hands puffy. When the fingers were compressed the return circulation was very sluggish. 
The lower extremities too were abnormally cold. The usual palpable vessels pulsated. 

V as omotor neurosis , chronic rubor , cyanosis and coldness of feet , especially 
in cold weather. 

L. C., age 20 years, female, married (Jan. 18, 1918), says that her right foot was frost¬ 
bitten some seven years ago. Since then her feet have always been cold and red, especially 
in cold weather. There is no pain. Seven weeks ago the little and great toes became 
cyanotic. There is a drawing sensation over the dorsum of the right foot. (None of the 
symptoms of thrombo-angiitis obliterans are present.) 

Physical examination reveals marked rubor of both feet, especially the right, whilst all 
the vessels pulsate normally. On leaving the limbs exposed for some ten minutes, they 
become somewhat cyanotic, the rubor diminishing. Ischemia on elevation is absent. 
Confirmatory examination one month later showed the same degree of rubor. 


CHAPTER CIII 

ATYPICAL VASOMOTOR NEUROSES 

In this group we may include a variety of atypical affections in which 
the symptoms consist of merely vasomotor disturbances or those associated 
with trophoneuroses, the larger arteries being demonstrably patent; yet 
the clinical picture deviates considerably from the Raynaud complex or 
from erythromelalgia . 1 

1. Localized Asphyxia with Arteries Pulsating. —Characteristic here are 
the presence of all the pulses, the absence of intermittent claudication, of 
ischemia on elevation, and even of reactionary rubor. This complex cannot 
be differentiated clinically from the type of thrombotic gangrene asso¬ 
ciated with healthy vessels described in Chap. XCVIII. Possibly an angio¬ 
spastic stage precedes the syndrome discussed as “thrombotic peripheral 
gangrene” (although the histories do not suggest it); and superinduced by 
cold or other insult, a stage of chronic cyanosis with gangrene results, the 
peripheral thromboses being secondarily induced. Here, because of the 
transitory and often evanescent nature of the affection, the existence of a 
pure neurosis is most probable. 

I. G., age 68, the little toe of the left foot had been cyanotic when she was admitted to 
the hospital in January, 1914. She had then complained of “sticking pain” in the toes for 
several weeks. On July 15, 1914, she returned with cyanotic discoloration of the adjacent 
toe, the toe formerly affected being practically normal. 

Physical examination: The fourth toe of the left foot is,deeply cyanotic and col,d, the 
adjoining sole also bluish. The fifth toe is negative. Pressure over the discolored toe 
elicits pain. No ischemia on elevation, no rubor, none of the usual appearance of thrombo¬ 
angiitis obliterans or arteriosclerosis; all the arteries pulsate. 

1 For Capillary Microscopy in the Vasoneuroses see Chaps. CVI, CVII et seq. 


ATYPICAL VASOMOTOR NEUROSES 


573 


O n July 27, 1914, a red area seemed to be extending from the base of the fourth toe 
toward the tip, suggesting that cyanosis was disappearing, yielding to reactive hyperemia. 
No further observations could be made after July 28, since the patient left the hospital. 

At first glance such cases might be mistaken for atypical Raynaud’s 
disease or atypical localized acroasphyxia. But from the former, they are 
distinguished by the involvement of one toe at a time, the lack of sym¬ 
metry , and the absence of paroxysmal attacks. From the latter affection there 
is even more marked deviation, both from the anesthetic and hypertrophic 
forms; the localization, the short duration, the absence of dystrophic processes 
stamp it at once as of wholly different nature. It properly belongs, there¬ 
fore, to an atypical or intermediary group of vasomotor neurosis. The very 
limited distribution of the cyanosis and the pain and tenderness are in con¬ 
trast with the more extensive cyanosis and the hypaesthesia of acrocyanosis. 

2. Rubor and Cyanosis.—Color changes of the lower extremities with or 
without slight edema characterize certain cases of vasomotor instability 
where the vessels pulsate and there are no evidences of arterial obliteration. 
The feet and legs tend to become reddish, then cyanotic in the pendent 
position. They may be colder than normal, and a play of colors with a 
marmorated appearance of the skin of the foot and leg my occur from time 
to time. 

A. G., female, age. 19, dates her trouble back to an attack of erysipelas 6 months pre¬ 
viously. She complains of having had some swelling of the feet even before this attack 
came on. Present complaint, discoloration and swelling of the legs with some pain along 
the inner aspect. 

Examined after standing, both feet are quite cyanotic. This color gradually disappears 
in the horizontal position, being replaced by a marked mottling (cutis marmorata) that 
extends up to a short distance above the knees. After manipulating the legs incident to the 
examination, the color of the left leg changes again, pinkish areas interspersed with cyanotic 
patches making a striking contrast. These changes also arise when the legs are at rest. 
All of the vessels pulsate strongly. 

3. Vasomotor Symptoms with Slight Trophic Disorders.—As vasomotor 
phenomena become associated with trophoneuroses, the cases approach 
erythromelalgia and Raynaud’s syndrome, although there are still a number 
of intermediate forms which belong to neither of the two latter clinical 
entities. 

Coldness, rubor, with ungual dystrophies and pain, especially nocturnal, 
make a picture not easily grouped with the well known and classical forms of 
vasomotor and trophic neurosis. 

B. S., female, 66 years of age, of neurotic disposition, had chilblains as a child, and since 
then cold feet in inclement and cold weather. For more than a year she has had pains in 
the feet and legs at night, is awakened and finds them red and glazed in appearance. 
Several weeks ago the big toe nail came off, and a new nail is appearing. The pain seems 
particularly present when trophic lesions appear and is reported as occurring when the leg is 
in the horizontal position. 

Examination reveals rubor of the foot, especially marked in the pendent position; the 
nails look ill nourished, the right big toe nail is new and growing in, the left appears dry, 
discolored and atrophic. All of the vessels pulsate. The symptoms disappeared completely 
after some 3 years. 

Differentiation from Erythromelalgia .—Although simulating this affection 
in the existence of rubor and pain, this atypical vasomotor neurosis fails to 
evidence the following characteristic marks of the Weir-Mitchell syndrome, 
namely: the combination of active hyperemia, redness, swelling with intense 
pain occurring in paroxysmal fashion; the dependence of the pain on the 
pendent position, on warmth, or on exertion, and the association of the hyper¬ 
emia with bounding pulsation of the arteries and venous dilatation. 


574 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


4. Vasomotor Neuroses as Prodromal Stage of Thrombo-angiitis 
Obliterans. —The frequent occurrence of thrombo-angiitis obliterans in 
Russian Hebrews should not, however, bias the clinical judgment to such an 
extent that the possibility of vasomotor neuroses is too strongly rejected. It 
is true that vasomotor symptoms may sometimes initiate the onset of organic 
arterial disease, making the differential diagnosis difficult, particularly when 
the palpable vessels all pulsate. An extended period of observation may be 
required to clarify the exact nature of a given case. The following instance 
is one in which we are dealing either with a case of vasomotor instability or 
with neurotic vascular manifestations antedating the typical signs of organic 
vascular disease. 

J. S., March 15, 1920, Russian, male, 48 years of age, complains of cold toes and fingers, 
particularly the toes of the left foot. He says that the toes become almost white at times, 
and when they are so, they are numb. With this there is severe pain, so that the patient 
under these circumstances is unable to stand or walk for any length of time. This trouble 
dates back some 6 or 7 years, but seems to be getting progressively worse. 

Physical examination shows that the vessels all pulsate, and none of the usual symptoms 
of thrombo-angiitis obliterans are present. 

Conclusion. Early involvement of peripheral vessels, such as the plantar arteries with 
occlusive thrombi, cannot be excluded here, although vasomotor symptoms dominate the 
clinical picture. 

5. Vasomotor Psychoneurosis. —This is an appellation that has been 
given (Donath 1 ) to certain types of vasomotor disturbance in which the 
vascular and sensory (painful) derangements bring about a psychic reaction. 

In a young man there had appeared for many years dark rose red, irregular, large patches 
over the skin of the face, cyanosis of the hands, rubor of the toes and soles of the feet. With 
the discoloration of the face there was occasional burning, prickling, pressure, and a feeling 
of tension. Warmth and emotional states increased the vasomotor phenomena. With 
this there was irritability, lack of desire to work, depression, and a melancholic state 
followed. 

6. Vasomotor and Trophoneuroses Following Infections. —We shall allude 
here merely to those instances of local vasomotor instability following local 
infections of the extremity, such as erysipelas, that have been referred to 
elsewhere, and to the similar neuroses of the vasomotor system subsequent 
to exposure to cold , 2 with or without infection. We are concerned in this 
group, however, more particualrly with those instances of angioneuroses that 
occur after severe general infections, such as typhoid fever. As an inter¬ 
esting example of acroparesthesiae and acroasphyxia we may cite the follow¬ 
ing (Heveroch 3 ). 

In a patient 26 years of age, after typhoid, there developed chronic cyanosis and frigid¬ 
ity of the lips, ears, hands, feet and legs, while evidences of vascular dilatation with rubor 
were present in the region of the tongue, skin of the breast and neck. The acroasphyxia 
was accompanied with paresthesiae and trophic ulcers. The reporter assumed that in this 
case disturbances of endocrine function, probably in the thyroid, were responsible for the 
vasomotor manifestations. 

7. Traumatic neuroses with vasomotor disturbances of the hands and 
feet are described by Oppenheim. These are characterized by intense 
swelling of the skin, cyanosis, abnormalities of temperature and alterations 
in the pulses. With motility undisturbed there are also secretory distur¬ 
bances such as hyperhidrosis or anhidrosis, and in rare cases, scleroderma-like 

1 Donath, Deutsch. Ztschr. f. Nervenh., 1920, 66, 83. 

2 Chapter on Thermic Gangrene, XXXI. 

3 Heveroch, Wien. med. Wchnschr., 1918, No. 33. 


CLINICALLY BORDERLINE CASES 


575 


changes in the fingers, nutritional disorders of the nails, local hypertrichosis 
and even bone atrophy. These manifestations have been observed with 
rather usual frequency during the Great War. When edema with cyanotic 
discoloration is present, a syndrome simulating that of certain hysterical 
manifestations may develop. This must be differentiated from that symp¬ 
tom-complex of cyanosis and edema produced by the malingerer, in his 
attempt to arrest the circulation of a limb by tight constricting cords or 
bandages. 


CHAPTER CIV 

CLINICALLY BORDERLINE CASES 

The vasomotor neuroses frequently afford clinical complexes of a border¬ 
line type, in that their manifestations may belong to more than one of these 
diseases. Properly speaking, such borderline cases do not occur amongst 
the organic vascular diseases. Whereas the vasomotor neuroses are grouped 
and classified on clinical grounds alone, we are in possession of sufficient 
knowledge to easily differentiate the various organic vascular varieties. The 
term “borderline cases” of organic type may, however, be extended so as 
to include those in which the existence of arterial closure cannot be deter¬ 
mined. In these the symptoms do not warrant a positive conclusion that 
narrowed or closed arteries are at hand, since physical evidences thereof 
escape our interpretative powers. 

We may describe two varieties of borderline cases. 

Firstly, those that are evidently neurogenic, but in which the symptoma¬ 
tology does not allow of a positive separation into the usual entities that 
clinical experience has enabled us to recognize and segregate. 

Secondly, borderline cases in which organic lesions cannot be excluded, 
and which in their clinical signs partake rather of vasomotor diseases. 

Whilst the interpretations of the former type may give the inexperienced 
observer some difficulty, the associated symptoms are not so intricate as to 
be particularly perplexing. We need not dwell on these since they are 
discussed elsewhere . 1 However, where no evidences of arterial occlusion 
are present, and the suspicion of organic arterial disease is still warranted, 
we are confronted with a different problem. 

Experience has shown, as well as our pathological studies, that there are 
two vascular territories prone to obturative alterations, capable of producing 
a variety of symptoms and manifold lesions. Such obstructive lesions can 
only be assumed as existing in those instances in which certain clinical 
manifestations would remain unexplained upon other grounds. These 
territories are the digital and the plantar vessels. In the description of 
thrombo-angiitis obliterans, a number of types have been cited, in which 
it has been proved beyond peradventure, that there was an earlier period in 
the clinical course in which the symptoms could not be explained with 
certainty; but that thereafter, by virtue of an ascending occlusion into the 
dorsalis pedis and posterior tibial, the prior existence of occlusive lesions in 
the aforementioned vessels could be taken for granted. 

1 See Chaps. LXXXVII, CVII and CVIII. 


576 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


And so we have learned that occlusive lesions in these non-palpable vessels 
occupy one of the early stages in some cases of thrombo-angiitis.obliterans. 
The accompanying manifestations therefore, must be differentiated upon 
other signs, for all the palpable arteries will pulsate. It has been already 
pointed out that important in the recognition of thrombo-angiitis obliterans 
is the localized pain, the developing ischemia, the history of migrating 
phlebitis, the induction and development of erythromelia and of ischemia, 
and a number of other valuable features. 

It is rather paradoxical, that in spite of the absence of certain knowledge 
regarding the situation of the fundamental lesions in the neurogenic vascular 
affections of the extremities, it is comparatively less difficult to satisfactorily 
group these affections for the inexperienced observer, than is the correct 
separation of the organic types from each other, or from the vasomotor forms. 

There are cases with predominating vasomotor symptoms that are but 
the forerunners of the usual picture of organic obliteration of the deep vessels 
of the extremities. In such, a differential diagnosis may be impossible, and 
extended observation is necessary for accurate diagnosis. Some of these will 
eventuality be diagnosticated; in others, by reason of inadequate opportunity 
for clinical study, we may fail to recognize the true malady. We shall cite a 
number of examples and point out in what manner a correct interpretation 
of the disease can be arrived at. 

From the diagnostic standpoint such cases group themselves into two 
classes: firstly, those that present vasomotor symptoms that are later shown 
to have been the forerunners of organic vascular disease; and secondly, those 
in which the diagnosis is in doubt, for no subsequent observations are at 
hand to convincingly establish the nature of the affection under observation. 

i. Cases of Incipient Thrombo-angiitis Obliterans with Apparent Vasomotor 
Symptoms . 1 —The symptoms vary considerably. Some have pain in the 
foot or fingers, particularly at night, rubor, cyanosis and coldness being the 
significant signs, the usual vessels pulsating strongly. At first there may be 
no evidence of arterial obstruction, in that ischemia is absent on elevation. 
If the case be observed, however, ichemia on elevation of the foot will develop 
either in all of the toes of one foot, or in one or more toes alone. The process 
may involve one or both feet to a varying extent and degree. 

The characteristic differences between pure vasomotor diseases and early 
prodromal vasomotor manifestations of thrombo-angiitis obliterans are that 
in the former, the evidences of neurotic derangement continue almost 
unchanged except for the possible development of gangrene; in the latter, 
however, continued observation will be rewarded by the appearance of 
manifestations attributable to obstructing vessels alone. These are blanch¬ 
ing on elevation of the limb, even though confined to a single toe, and finally 
the loss of one or more of the palpable pulses. 

Early thrombo-angiitis obliterans. Apparent vasomotor symptoms at the 
onset , all vessels pulsating , later development of ischemia on elevation. 

N. K., Russian Hebrew, 38 years of age, consulted the author, December 3, 1911, with a 
history of having had pain in the leg for about 3 years. About 6 months ago the fifth toe of 
right foot became rather bluish, and then he developed pain in the entire right foot. 
The fourth toe of the left foot also began to hurt him, the adjacent third toe having occasion¬ 
ally given him similar trouble. The pain has increased so of late that it interferes with 
walking and persists during the day, as well as at night. 

1 Similar cases in which the further course could not be followed and in which a funda¬ 
mental organic basis could not be demonstrated, are described under vasomotor tropho¬ 
neuroses. 


CLINICALLY BORDERLINE CASES 


577 


Physical examination: The fourth toe of the left foot is cyanotic, there being patches of 
scarlet red interspersed with bluish areas. All the other toes of the left foot are slightly 
cyanotic and the whole foot is somewhat cold. The fifth toe of the right foot is also 
cyanotic. All the vessels of both extremities pulsate strongly. After a prolonged stay in 
the pendent position, the feet become cyanotic and there is no definite evidence of blanching 
on elevation. 

Subsequent observation strengthened the view that in spite of the apparent patency of 
the larger palpable vessels, the case was one of thrombo-angiitis obliterans. 

December n, 1911, further note: The ankle of the right foot is particularly painful. 
He says that the toes of the left foot become red and swollen. Examination shows that the 
toes of the right foot tend to become cyanotic. In the pendent position there is no rubor 
or erythromelia, but increasing cyanosis. Both feet are cold, particularly the 
forepart of the right foot. On elevation there is an absence of ischemia. There are no 
trophic disturbances. 

December 26, 1911: Patient complains of intense pain. Now the third, fourth and fifth 
toes of the right foot are markedly ischemic. Ischemia can also be elicited oii elevation. 
All the vessels pulsate. 

In short, a patient, in whom at first no absolute evidence of thrombo¬ 
angiitis obliterans could be elicited, develops localized ischemia on elevation 
and without elevation, strongly suggestive of an obturating disease of the 
vessels. 

2. Cases with Developing Ischemia , Probably Thrombo-angiitis. 

P. A., 32 years of age, Austrian Hebrew, consulted the author on the 8th of October, 
1917, and complained of pain in the arches of the feet radiating to the knee, this having 
been present for about 2 years, and becoming progressively worse. For the last 6 months 
she has been able to walk only about 20 minutes, because of the increasing intensity of the 
pain. The feet are always cold, and when sitting they feel numb. She cannot stand 
longer than 5 minutes at a time. 

Examination shows that all the vessels of both lower extremities pulsate well. There is 
marked cyanosis of the feet in the pendent position, no ischemia on elevation. 

In short, a history of vague pain, possibly intermittent claudication, 
cyanosis of the feet, absence of ischemia, all the vessels pulsating. 

However, during a period of observation lasting for 3 weeks, it was 
noted that evidences of distinct blanching upon elevation of the feet over a 
period of 5 minutes or more could be obtained. 

Thus, on the 25th of October not only did blanching develop, but slight 
or moderate reactionary rubor. 

These developing signs were sufficient to stamp the case as one of thrombo¬ 
angiitis obliterans. 

3. Cases with Cyanosis Resembling Arocyanosis . 1 —-Just as a preponderat¬ 
ing rubor may give the clinical picture simulating erythromelalgia, so when 
cyanosis of the toes is marked, a clinical picture suggestive of acroasphyxia 
may be produced. 

In favor of thrombo-angiitis obliterans and against the atypical vasomotor 
derangement, besides the advent of ischemia and obliteration of the pulses, 
is the symptom of pain. When the pain is severe and localized in one or more 
toes and persists over a considerable period of time, it is strongly suggestive 
of organic obliteration of the vessels. In acrocyanosis (chronic acroasphyxia) 
hypesthesia or anesthesia is more apt to be characteristic. 

Doubtful case with cyanosis of the toes as chief symptom. 

B. S., seen April 25, 1913, 51 years of age, Roumanian, complained of pain in the sole of 
the right foot after exertion, but which did not give him particular concern until 8 weeks ago. 

About this time the pain in the sole of the right foot became more severe, but there was 
no discoloration. One month ago he was advised to wear flatfoot inlays. Shortly there¬ 
after the second and third digits of the right foot began to swell, later becoming bluish in 
color, this discoloration persisting up to the present time. 

1 Excruciating pain in one toe may signalize the edvent and the destructive results of 
localized vasoneurotic necrosis (See paragraph 5, p. 578). 

37 


578 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Physical examination: The right foot is slightly swollen, and there is distinct cyanotic 
discoloration of all the toes. All the vessels pulsate well. There is no ischemia and there 
are no trophic disorders. 

4. Cases with Limited Asphyxia and with Pain. —Pain localized in one or 
more toes with asphyxia and coldness of these may, in coexistence with pulses 
everywhere present, form a syndrome difficult of interpretation. We are 
confronted in these with the problem of differentiation between (1) thrombo¬ 
angiitis obliterans with restricted peripheral vascular involvement of plantar 
and digital arteries; (2) post-thermic vasomotor derangements (especially 
after exposure to cold); (3) chronic acroasphyxia with pain as an unusual 
feature; (4) atypical Raynaud’s disease; and (5) bland thromboses of small 
peripheral vessels of varying etiology (arteriosclerosis). 

Citation of a case observed in an elderly woman will elucidate. The 
diagnosis may be impossible unless data from a sufficient or extended period 
of observation are at hand. Here peripheral thrombosis engrafted upon 
intensive arteriosclerotic lesions is the most probable pathogenesis. 

I. G., Russian female, aged 68, was admitted to the hospital July 15, 1914 complaining of 
discoloration of the fourth toe of the left foot, and sticking pain and tenderness of all the 
toes and soles of both feet. There had been a similar condition present 7 months prior with 
discoloration of the fifth toe of the left foot, which had subsided. 

Physical examination shows an arteriosclerotic patient, whose left leg appears 
normal except for intense cyanosis of the fourth toe. Pressure over this toe elicits consider¬ 
able pain. On elevation of the foot, the toe becomes slightly paler, although there is no real 
ischemia of the foot. There is no erythromelia in the pendent position, and the foot has 
not the typical appearance of arteriosclerosis or thrombo-angiitis obliterans. All the 
arteries pulsate. 

July 27, 1914. A red area seems to be extending from the base of the fourth toe towards 
its tip, indicating possibly that cyanosis is disappearing and active hyperemia is being 
established. Since the patient refused to remain in the hospital, she was discharged 
unimproved. 

Conclusions. —The absence of paroxysmal attacks, the constancy of the 
cyanosis, the lack of symmetrical involvement of both feet, the developing 
local rubor—all seem to point rather to an organic affection of the arteries 
rather than to a vasomotor neurosis. Nevertheless, an atypical form of 
Raynaud’s disease cannot be excluded. 

5. Vasoneurosis and Organic Arterial Disease. —Most interesting are the 
cases with frank arteriosclerotic disease of the vessels of the lower extremities, 
in which attacks of asphyxia and pain in a toe rapidly lead to superficial 
gangrene. These occur most frequently in elderly women, and the absence 
of pulsation in the dorsalis pedis and posterior tibial arteries may lead to 
the erroneous conclusion that all trophic disturbances of the necrotic type 
must necessarily be caused by obliterative conditions of the arteries. It is 
not easy to evaluate the comparative etiologic forces at work. Do vaso- 
neurotic abnormalities of function play a role at all; or, is thrombosis in 
small, digital vessels responsible? Cases of the thrombotic type do occur, 
as previously described (p. 480); but our experience warrants the belief 
that neurogenic arterio- or venospasm may lead to necrosis in the above-mentioned 
cases independent of the condition of the larger arteries. 

This may be accepted as correct for the following reasons; and the explana¬ 
tion may serve also to differentiate the cases of purely organic, peripheral 
necrosis, from combined organic vascular disease and vasomotor neurosis. 

(1) Although the dorsalis pedis and posterior tibial arteries are pulseless, 
the general nutrition of the limb shows no marked evidence of deterioration! 


TREATMENT OF VASOMOTOR NEUROSES 


579 


(2) The color of the feet may be good, ischemia on elevation may be 
absent. 

(3) The necrosis is usually limited to a patch of skin at the tip of the toe, 
the circulation (color, etc.) throughout the rest of the digit apparently good. 

(4) Acupuncture at the base of the affected toe yields just as copious 
bleeding as in other toes at similar sites. This would seem to indicate that 
the circulatory deficiency is no greater than in other toes, and that the gan¬ 
grene follows local abnormalities of circulation—most probably vasoneurotic 
in nature. 

Capillary microscopy of the subpapillary capillary circulation in the 
region of the affected cutaneous area should show evidences of vasoneurosis, 
such as spasm, atony and distortion of capillaries. 

The clinical history of a typical case maybe thus summarized: A patient 
over 50 years of age (usually female) who has been regarded as having sclero¬ 
tic arteries, has had attacks of pain and blueness of one or more toes over 
periods of months, the paroxysms of variable length, not symmetrical, 
and without any previous syncope, gradually subsiding without necrosis. 
A more severe attack supervenes, one that distinguishes itself from the pre¬ 
ceding in that an affected toe, possibly of the other foot, soon shows a patch 
of permanent purplish discoloration. The pain becomes more and more 
intense; finally, the superficial skin is lifted off over the center of the cyanotic 
area by accumulating fluid, and removal of the epidermis discloses bloody 
or purulent serum. Following or without the use of the Leriche operation 
of decortication of the femoral artery, but aided by detachment of the dead 
epidermies and multiple puncture of the exposed corium, gradual restitution 
takes place. The rest of the toe is practically normal. 

Such, in short, is a clinical example of vasoneurosis with tissue death, 
associated with organic arterial disease, a complex in which a differential 
diagnosis between the effects of pure arterial obliteration and of superadded 
neurogenic functional abnormalities may be difficult or impossible. 


CHAPTER CV 

TREATMENT OF VASOMOTOR NEUROSES 

However appealing the vista of ideas that modern pharmacology has 
revealed concerning the specific action of certain substances on the vegetative 
system, but little of practical value has as yet arisen in the treatment of the 
vasomotor neuroses. Nevertheless a knowledge of some of the principles 
and the fundamental reactions and susceptibilities of the sympathetic 
system to drugs is essential, if we would make progress in our therapeutic 
endeavors. 

Reference has already been made in the chapter on the Vasomotor 
Nervous System concerning the specific action of nicotin; that it paralyzes 
all the nerves of the vegetative system of both sympathetic and autonomic 
origin, but that this effect is exerted especially at the relay station between 
preganglionic and postganglionic fibers. A ganglion of the vegetative 
nervous system when painted with a weak solution of nicotin (Langley) is 
incapable of responding to excitations through central or preganglionic paths. 

There are poisons that have a selective action, in that some exert a 
special and exclusive influence either on the sympathetic or parasympathetic 


580 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


systems. Indeed, through pharmacologic methods, the differentiation of 
the parasympathetic and sympathetic systems becomes possible. 

Poisons of the cholin group cause excitation of the terminal apparatus 
of the parasympathetic system. Muscarin, physostigmin and pilocarpin 
also belong to this group. Thus pilocarpin furthers secretion and excites 
spasm (lachrymal secretion and miosis). The atropin group paralyzes the 
end filaments and hence secretion is inhibited and abolishes spasm (cessation 
of lachrymal activity and mydriasis). 

The bronchial muscle spasms are usually treated with atropin in order to 
paralyze the bronchoconstrictor fibers in the vagus. So, also, in spastic 
ileus, the same drug is employed. 

Other drugs act exclusively on the sympathetic nerve system, as adrenalin. 
All terminals of the sympathetic nerves are stimulated by this substance or 
its synthetic substitutes. And so, adrenalin has particular value as a vaso¬ 
constrictor and to control hemorrhage. Conversely, this drug excites the 
bronchodilators and is of value in bronchial asthma. 

It is believed that there is a special chemical affinity between certain 
poisons and the affected nerve endings. 

The following scheme adapted from Muller 1 summarizes the specific 
actions of certain substances. 


The Sympathetic System 


A. IS STIMULATED BY ADRENALIN WHICH 

Excites the nerve endings, 

Dilates the pupils, 

Causes vasoconstriction, 

Causes piloerection, 

Accelerates the heart beat, 

Dilates the bronchi, 

Inhibits the gastrointestinal muscu¬ 
lature. 


B. IS PARALYZED BY ERGOTOXIN WHICH 

Causes vasodilatation, 

Retards the heart (through paralysis of 
the vasoconstrictors and of the 
accelerators). 


Because of our lack of knowledge as to the pathogenesis of the vasomotor 
and trophoneuroses, an effective causal therapy has not as yet been proposed. 
For purposes of better orientation as to the line of thought that the 
student should follow in his attitude towards the therapy of these affections, 
some of the newer observations on the role of certain salts in modifying the 
excitability of the nervous system may be reviewed here. 

In spasmophilic conditions, such as tetany, a withdrawal of calcium from 
the body fluid has been noted (MacCallum and Vogtlein 2 ). The symptoms, 
however, are not primarily due to the altered calcium balance, since para¬ 
thyroid deficiency is responsible both for the change in the creatinin (guani- 
din), as well as for the disturbed calcium metabolism. Indeed, tetany has 
been described as poisoning with guanidin bases (Farner and Klinger 3 ). 
According to these observers these poisons are taken up, destroyed and 
oxidized by the cells of the epithelial bodies. In consonance with this 
theory the degree of toxic symptoms would depend upon the amount of 
parathyroid tissue and upon the quantity of toxic bases in the circulation. 

Following this line of reasoning the disturbance in the calcium metabolism 
would be a sequence, and calcium therapy would only partially modify the 

1 Muller, Das vegetative Nervensystem, Springer, Berlin, 1920. 

2 MacCallum and Vogtlein, Jour. Exper. Med., 11, p. 818; also 20, p. 149. 

3 Farner and Klinger, Grenzgeb. d. Med. u. Chir., 1920, 31, p. 469. 


TREATMENT OF VASOMOTOR NEUROSES 


581 


result of the endocrine deficiency. But when there is a dearth of calcium in 
the blood in tetany, this may be the effect of calcium deionization through 
acid, and consequently calcium administration would only nullify or neu¬ 
tralize a secondary sequence of the endocrine disturbances. 

Enough has been said, to call attention to the fundamental premises 
upon which the administration of certain salts may be based; and with these 
some therapeutic success has been reported. 

That a similar mechanism of endocrine disturbance may be a fault in 
some of the vasomotor neuroses has already been suggested. Another reason 
for the belief in the administration of calcium is its influence on the nervous 
system. Pharmacologically it has been shown that withdrawal of calcium 
increases the excitability of the vegetative nervous system, as well as the 
cerebral spinal motor nerve endings through the action of certain poisons 
'(Chian and Frohlich 1 ).. Calcium also has an antagonistic action to muscarin, 
which is known to excite the parasympathetic system. In short, calcium 
may be regarded as having a narcotic action (Lowi 2 ) upon the nerve elements, 
both central and peripheral. Hence, its value in spasmophilic conditions, 
for which large doses of calcium chlorid per os, or by intravenous adminis¬ 
tration have 1 been advised. 

Calcium has been extensively used recently in disturbances of the vege¬ 
tative nervous system. Two distinct effects have been observed after its 
administration: firstly, an acute one after intravenous injection, which mani¬ 
fests itself in an accentuated or exaggerated reaction to sympathetic exci¬ 
tants; and secondly, a more prolonged effect which results from improved 
central regulation of the vegetative function. 

According to this view (Dresel) calcium injections would have a field of 
application whenever we desire to increase temporarily the sympathetic over 
the parasympathetic excitability (therefore, in cases such as bronchial asthma, 
which demonstrate an increased tonus in the vagus). Such injections, 
however, have but a fleeting effect. 

In those conditions where the regulatory mechanism in the vegetative 
centers is chronically disturbed and reacts inordinately to psychic, metabolic 
or other influences, calcium therapy is believed to be of value. To what 
extent this drug will be useful in the vasomotor neuroses, only more extensive 
trial than has been heretofore given, can establish. Intravenous injection of 
calcium chlorid in 5 to 10 per cent solutions, in doses of 2 to 10 cc., have been 
employed. For the permanent effects, administration per os in sufficient 
amounts is to be recommended. 

Surgical Treatment. —Leriche 3 advises an operation of denudation of the 
larger arteries of a member that is supposedly affected with symptoms due to 
sympathetic nerve disturbance. The procedure is based on the theory that 
irritative impulses are responsible for the symptoms. Certain clinical and 
physiological facts are believed to afford the anatomic basis for such an opera¬ 
tion. These are: firstly after operation on or removal of the sheath of an 
artery > the vessel contracts; secondly, pulsation of the vessel stops, and thirdly, 
the size of the vessel diminishes. When the periarterial connective tissue, is 
removed, the artery becomes one-third or one-fourth of its normal size, 
while on both sides of the denudation its caliber is normal. The consequent 
arterial contraction causes disappearance of the pulse without altogether 
interrupting the circulation. 

1 Chiari and Frohlich, Arch. f. exper. Path. u. Pharmakol., 64 and 65. 

2 Lowi, Arch. f. exper. Path. u. Pharmakol., 70, p. 323; 82, p. 131. 

3 Leriche, Ann. Surg., Oct., 1921, Vol. 74. 


582 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Immediately after this procedure the pulsation is imperceptible or feeble, 
the limb becomes colder than the opposite one, and the temperature becomes 
lower. Subsequent to this the following reactionary phase ensues with: 
firstly, elevation of local temperature 2 to 3 0 above normal and a subjective 
sensation of heat; secondly, elevation of the arterial pressure, and thirdly, 
increased amplitude of oscillations as shown by the sphygmomanometer. 
The reaction of vasodilatation after periarterial sympathectomy becomes 
weak after the fifth or sixth day and disappears after 3 to 4 weeks. 

Leriche believes that in traumatic vascular spasm 1 there occurs an active 
vasoconstriction through excitation of the periarterial layer. Such cases, as 
well as some of Raynaud’s disease, might in his opinion respond to the 
operation of denudation. 

Certain characteristic signs are said to follow cutting the periarterial 
sympathetic nerve. The responses are described as being primary and 
secondary. 

The primary reaction of sympathetic nature is a vasoconstriction follow¬ 
ing manipulation of the artery; this may attain such a degree as to reduce 
the arterial diameter to one-third or one-quarter of its normal, and involves 
all of the denuded segment. The adjacent parts of the artery retain their 
normal caliber. The rapidity of the reaction varies in different arteries and 
according to the susceptibility of the individual. The constriction is said 
to be stronger in arteries of middle caliber than in the larger trunks.. The 
reduction in size of the lumen may be sufficiently great to cause the pulse 
to disappear, but all of the circulation is not thereby abolished. 

Some of these observations are in consonance with those of the author 
and of others, on the arterial spasms occurring when the radial artery was 
prepared for the direct transfusion method. These phenomena were 
observed in the days when the artery and vein were connected by suture or 
by cannula. They are also in accord with data on the so-called traumatic 
vasomotor spasm described in another chapter. 

Immediately following the operation, the peripheral pulse becomes 
imperceptible or very feeble, and the part colder than the other. A char¬ 
acteristic physiological reaction gradually appears either at the end of 3 or 
6 hours, more frequently after 12 or 15 hours. This reaction (secondary 
response) is characterized by an elevation of the local temperature (2 to 
3 0 C.), an increased arterial pressure, and an augmentation of the ampli¬ 
tude of the oscillations. This vasodilating reaction is only transitory, for 
the hyperthermia and the elevation of pressure gradually diminish; and, after 
2 weeks, these changes disappear. 

The Operation .—The artery is isolated over a distance of from 9 to 10 
cm., the sheath is opened and the cellular tissue dissected away from the 
vessel without injury to the arterial wall. 

Leriche states that the operation failed in intermittent claudication; in 
one case of trophic disorder after frost-bite; in one case of spasmotic para¬ 
lysis; and in certain cases of painful syndromes like erythromelalgia. The 
author summarizes his experiences as follows: 

1. In painful phenomena sympathectomy was often very efficacious. 
In causalgia after war wounds he reports two complete failures, two cases of 
improvement and five excellent results. In the painful conditions preced¬ 
ing gangrene of obliterating endarteritis with or without intermittent claudi¬ 
cation good results were recorded. In two cases of Raynaud’s diseaseJ:here 
were good results. 

1 Leriche, Presse Med., Sept. 10, 1917, p. 513. 


TREATMENT OF VASOMOTOR NEUROSES 


583 


2. The hypertonic symptoms in certain muscular phenomena complicat¬ 
ing war injuries were well influenced. Eighteen patients were very much 
improved; the contractures ceased and voluntary movements became 
possible the day after operation. 

3. In trophic ulcers sympathectomy was found efficacious, but not in 
perforating ulcers. 

4. In cases of trophic symptoms after nerve section good results were 
recorded. 

Sufficient data are not yet at hand to establish the indications, or to 
definitely evaluate the worth of this procedure. The criticism that there 
exists but inadequate fundamental anatomic basis therefor, has been 
mentioned elsewhere (Chap. IV). Nor has most recent experimental work 
(Lehman 1 ) succeeded in demonstrating improved wound healing as a 
sequence of the vasodilatation brought about by this operation. 

The Role of the Sympathetic in Certain Pathologic Conditions. —Those who 
have done periarterial sympathectomy claim that on the basis of results 
obtained, a number of clinical complexes can be interpreted as due to sympa¬ 
thetic disturbances. Thus, the following conditions were brought into causal 
relationship with the sympathetic nervous system. 

(1) Closed (contused) wounds and traumata of the arteries. 

(2) The causalgias. 

(3) The reflex contractures of the Babinski-Froment type. 

(4) Certain contractures at the elbow. 

(5) Certain motor paralyses following arterial lesions. 

1. Closed Wounds of the Arteries. —Arterial vasoconstriction may play 
a role in the arrest of hemorrhage, when arteries are injured by projectiles. 
The immediate result of periarterial sympathectomy is in direct harmony 
with the clinical observations of arterial contraction after injury. 

2. Causalgia and the Sympathetic. —Leriche believes that rebellious 
cases can be influenced by excision of the arterial sympathetic. In certain 
nerve injuries implication of adjacent sympathetic fibers is said to be respon¬ 
sible for the severe pain. In other words, the painful phenomena are not 
consequent upon sensory nerve lesions, but due to coincidental involvement 
of neighboring sympathetic fibers. Some of the painful affections apparently 
due to peripheral nerve lesions are, more properly speaking, reactions to 
derangement of the arterial sympathetic paths. 

3. The Role of the Sympathetic in the Reflex Contractures of the Babinski- 
Froment Type. —In this clinical complex vasomotor and thermic phenomena 
are associated with motor disturbances and modifications in the mechanical 
excitability of the muscles. These are said to completely disappear after 
periarterial sympathectomy. Even hands that have been fixed in an 
unchanging position were seen to resume their mobility when the fingers 
were contracted down into the palm. 

4. The Sympathetic in its Relation to Certain Contractures at the Elbow .— 
Here periarterial sympathectomy about the brachial artery was followed by 
successful results, even after resection and suture of the cut nerves of the 
forearm had failed. 

The Relation of Muscular Contraction and the SympatheticA —Certain 
muscular contractions seem to be dependent upon the sympathetic nervous 
system. It is believed that for the accomplishment of voluntary motion, 

1 Lehman, Ann. Surg., Jan., 1923, 77, p. 30. 

2 These observations represent the views of the French school. 


584 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


the integrity of the motor nerve apparatus and of the muscles alone does not 
suffice for the correct accomplishment of wilful motion. If the sympathetic 
nerves are involved or if their function is disturbed, the muscle hardens, 
becomes contracted, and voluntary relaxation and contraction may be no 
longer possible. Leriche claims that sympathectomy (periarterial) makes 
a progressive restoration of voluntary motion possible. In wounded soldiers 
with reflex contractures of the Babinski-Froment type, with immobile 
fingers, the operation of sympathectomy succeeded in restoring voluntary 
motility. The functional results do not appear to be due to a direct effect 
upon the muscles, but to some alteration in the vasomotor innervation. 
For, return of motility coincides with the appearance of post-operative 
vasodilatation, namely, simultaneously with the increased warmth of the 
muscles and its improved circulation (Heitz). 1 

5. Motor Paralyses Following Arterial Lesions .—In cases of Volkmann 
contracture, Heitz and Leriche report disappearance of vasomotor distur¬ 
bances, and diminution in the intensity of the trophic disorders after peri- 
arterial sympathectomy. 


CHAPTER CVI 

CAPILLARY MICROSCOPY 

Through the excellent work of O. Muller, and his assistants, E. Weiss, 
Parrisius and Niekau, our knowledge of the physiology and pathology of the 
capillaries of the surface of the body has become greatly amplified. 2 For the 
student who wishes to apply the methods of capillary microscopy in his 
clinical interpretations of deviations from the normal capillary function, a 
consideration of the facts herein given may be of value. 3 They will supple¬ 
ment the elementary facts given in Chap. VIII. 

Anatomical Considerations.—Through the studies of Weiss and Muller 
it was found feasible to illuminate the cutis by the methods previously 
alluded to (Chap. VIII), and to visualize the capillaries through the 
horny layer, the germinative layer of the epidermis, and the papillae, down 
to the subpapillary vascular network of the .corium. For a better under¬ 
standing of what can be thus seen, we shall give a brief account of the histology 
of the skin, insofar as the vascularity thereof interests us. 

The human skin is composed of the cutis and epidermis. The latter 
overlies the corium that gives rise to the nails and hair. The cutis is com¬ 
posed of the corium and subcutaneous tissues. 

The superficial.layer of the cutis—the papillary stratum—underlies the 
epidermis and presents a plain surface in the foetus. Later on it attains an 
undulatory surface composed of rows of papillae. The latter contain the 
loops of blood capillaries from about 0.03 to about 0.25 mm. in altitude. 
In certain portions of the body (volar surface of the hands and plantar of the 
feet) the papillae are arranged in rows and form wedge-like prominences 
(Fig. 169). 

1 Heitz, Soc. de Biologie, Feb. 17, 1917. 

• 2 Die Kapillaren der menschlichen Korperoberflache, Enke (Stuttgart), 1922. 

3 Some of the beautiful drawings of O. Muller have been reproduced. Nowhere else in 
the literature are such exquisite pictures to be found, and a few selected examples may be 
of value. 


CAPILLARY MICROSCOPY 


585 


, *Vascularization of the Skin .—If we refer to Fig. 170 (Spalteholz and 

Muller), the arterial and venous supply of the integument fall into four 
groups, first, a cutaneous, venous, and arterial network (rete artiosum 
cutan and rete venosum); second, an inferior subpapillary arterial and 
venous network; third, a superior subpapillary arterial and venous network; 
and fourth, venous and papillary loops in the papillary layer. The cutaneous 



Fig. 169. Cutaneous ridges and papillae containing capillary loops with parallel venous 
and arterial risers shown. ( Muller) 



Fig. 170. —Schematic drawing depicting vascular distribution in the skin. ( Muller) 

vessels approach the surface from the depth and form an anastomosing arte¬ 
rial network in the boundary zone between the subcutaneous tissues and the 
cutis. From this, branches of supply penetrate the subcutaneous layers. 
This cutaneous network is composed of direct anastomoses between the 
supplying vessels and secondary anastomoses between the vessels in the 
interstices. Up to the middle of the cutis, the arteries still possess distinct 






586 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


muscle layers, but in the subpapillary region only endothelium is present in 
the capillaries. Just below the base of the papillae the vascular risers are 
two in number, running in the direction of the long axis of the cutaneous 
ridges. From these vascular risers the arterial branches of the capillary 
loops ascend up to the tips of the papillae (Fig. 169), and the venous portions 
of the loops descend down to the level of the vessels of supply. Between 
the arterial and venous risers there do not appear to be any anastomoses. 

In view of the fact that the epidermis and the cutis can be made trans¬ 
lucent, Muller, with the special methods of illumination advised by him and 
to be described later, states that one can visualize the capillaries in the 
papillae down to a level almost corresponding to the base of the papillae, as 
indicated in Fig. 171 at the level IV. 

Apparatus for Visualization of Capillaries. —Muller has constructed a 
modified microscope (Zeiss) which is simple and useful for investigation of 
capillary flow. The instrument (Fig. 172) consists of a microscopic tube 
( t ) at the objective end of which (b) there is a small circular opening ( b ). 



Fig. 171.—Schematic cross section of skin showing depth ( IV ) of possible illumination. 

( Muller ) 

This opening is placed in contact with a portion of the integument selected 
for examination, a layer of cedar oil covering the latter. By means of a small 
lamp (e) oblique illumination is obtained. A second microscopic tube (//) 
serves for observation, the focus being controlled by the micrometer screw 
( m ). With a combination of lenses, an ocular ( ok ) and an objective ( ob ), a 
magnification of six times is possible. 

For a section of the skin of the trunk or upper portions of the extremities, 
the tube from 0 to ok comprises all that is necessary. To visualize the margins 
of the nail it is advisable to employ a stand ( st ) to which the microscope is 
attached by a screw (sch), a horizontal plate ( r ) being supplied with a 
depression to receive the finger. 

The Normal Flow in the Capillaries .—With the apparatus previously 
described (Fig. 172) the flow in the capillaries is usually found to be con¬ 
tinuous, in that discreet blood corpuscles cannot be distinguished (Fig. 181). 
Only at the point of transition from the arterial into the venous limbs is it 
possible, even in the normal, to note a lack of continuity in the blood column. 
From time to time one or another loop shows an arrest of the flow. As the 
normal stream becomes retarded, the usually continuous column of blood 
corpuscles becomes interrupted, and the so-called phenomenon of granular 
streaming becomes apparent (Fig. 173). Clumps of blood corpuscles may 
appear separated by light hiatuses of plasma. The stream may become more 
and more retarded, and finally may cease and stasis result. 










CAPILLARY MICROSCOPY 


587 


Fig. 172.— Muller’s Zeiss apparatus for capillary microscopy. ( Muller ) 




Fig. 173.—Granular streaming in an area showing an abundance of capillaries; case of 

nephrosis. ( Muller) 




































588 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


Marked acceleration of the stream may also occur, especially in the 
vasoneuroses, in essential hypertonia and the nephritides when the latter do 
not show decompensation. 

It must be remembered, however, that the current in the normal is 
variable, and it is not unusual to find that a sudden void occurs in some of the 
capillary loops. So that it is difficult to decide just where the pathological 
begins, and these phenomena of stream interruption and variability may have 
but little significance. On the contrary, an unusual degree of constancy and 
continuousness of flow, with unusual regularity is regarded as pathological. 
This may occur as the result of poisoning (mercury), or in vasomotor palsies 
induced by poisons of infections. 

Capillary Activity and the Capillary Stream .—Many observations are 
at hand that would support the theory of independent contractility of 
arteries and capillaries. Weiss and Dieter in their observations on the 
capillary flow in the finger tips, observed that even after sudden arrest of 
circulation in the arm by a blood pressure cuff (Chap. VIII), some 31 
seconds elapsed before the capillary stream ceased. Spontaneous con¬ 
tractions of the capillaries are observed as the result of external factors or 
endogenous reflexes; or are apparently of spontaneous origin in the endo¬ 
thelium. As an example may be cited the experiment of Weiss in which the 
application of ice over the skin in the region of the brachial artery was 
followed by a total disappearance of the flow in the capillary loops of the 
finger. Mention may also be made, in this connection, of the reports of 
Laewen 1 concerning the occurrence of spasm of the capillaries in the foot in 
cases of arteriosclerotic necrosis. This observer applied ice to the sciatic 
nerve and was able to demonstrate the disappearance of the angiospastic 
condition thereafter. It would appear from his studies that the exclusion 
of nerve influences even in organic arterial affections was potent in over¬ 
coming peripheral spasmodic phenomena in the capillaries. 

The author has pointed out the frequent association of vasomotor 
abnormalities with the organic arterial disorders ( e.g . thrombo-angitis 
obliterans, arteriosclerosis). It is of interest, therefore, to note here that the 
nervous system may be directly implicated in these phenomena. 

Other authors have tried to demonstrate the autonomic contractile 
forces present in arteries and capillaries. So Magnus 2 showed that after 
expression of most of the blood from an upper extremity with an Esmarch 
bandage and the resulting compression of the brachial artery, a streaming 
in the capillaries of the finger tips still continued; that the capillaries evac¬ 
uated themselves of blood, and that the whole process continued over a con¬ 
siderable period of time. Further, the same author has given a beautiful 
demonstration of the autonomic activities of the capillaries in the following 
experiment: if a tourniquet be applied to the arm and by acupuncture a 
phenomenon of white dermatographia with a red peripheral reaction be 
elicited, these responses are made to disappear upon release of the bandage 
as soon as the reactive hyperemia sets in. Even after a period of forty 
minutes the original dermatographic reaction may be made to reappear, if 
the bandage be again applied. 

We have, therefore, two beautiful clinical demonstrations of the control 
of the peripheral circulation through the nerve paths, as well as through 
local autonomic forces. Similar responses on the part of the peripheral 
vessels have been described by the author in Chap. XL VI, p. 247. 

1 Laewen, Zentralbl. f. Chir., 1922. 

2 Magnus, Deutsch. Ztschr. f. Chir., 162, 1921, No. 1-2. 


CAPILLARY MICROSCOPY 


589 


But even in the normal, a sudden void may occur in the capillary loops. 
In the efferent limb there may be sudden ischemia, a contractile wave passing 
up to the venous loop. Stases may occur by virtue of spasm in the fine 
arterioles. Muller applied the term “spasm” to the contractile phenomena 
occurring in the papillary capillaries, whilst the result of contraction in the 
pre- or postcapillary territory, he described as stases. 

Although it has been shown that contractile phenomena do occur in the 
capillaries as well as in the larger vessels, we are not warranted in assuming 
that these expressions of function are generally in force as a component part 
of the circulatory mechanism. For, all one can conclude is that local 
conditions in one or another territory bring about contractions of the capil¬ 
laries from time to time. Indeed, at the tips of the fingers one is often com¬ 
pelled to wait for a long time until interruption of the stream through 



Fig. i 74.—Local asphyxia in vasoneurosis with interruption of continuity of venous limbs. 

Note progressive movement of spasm in venous limb ( a-f ). ( Muller ) 

constriction is observed. On the other hand, in the erect position , studies of the 
toes bring to light that stases are frequent. Indeed, the period during which 
good circulation is seen in the capillary loops is often of shorter duration than 
the periods of stasis; and this applies to every healthy individual. And so 
we must conclude that here, at least, spontaneous activity in the capillary 
territory is shown. Perhaps in the upright position, the intent is to aid the 
circulation in the following manner: as the contraction occurs in the sub- 
papillary territories with consequent exclusion of the current in certain 
capillary loops, the flow must pass from arteries to veins in the deeper and 
larger communications (a shorter circuit). 

Whatever may be the mechanism by which this is accomplished, it 
seems well proven (Muller) that considerable territories of the papillary 
capillaries are at rest (constricted) in the standing position, with occasional 
opening of the latter for the purpose of insuring nutrition. 

Other interesting observations are at hand regarding the contractions 
that may occur in the peripheral capillaries. Some of these remind one of the 
peculiar phenomena of capillary circulation in the vasoneuroses, and espe¬ 
cially derangements that are associated with disturbances of internal secre¬ 
tion. Thus, certain authors have pointed out the changes in the capillary 
circulation during pregnancy (Lennartz 1 ). Stases in the circulation of the 
finger occur frequently during gravidity, and the capillary form and caliber 

1 Lennartz, Pfluger’s Arch. f. d. ges. Phys., 191, 1921, p. 302. 


590 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


undergo changes, such as dilatation of the venous limbs and elongation of the 
loops. 

Active motility in the capillary wall is also observable in the vasoneuroses 
(Chap. CVII). Here and there may be seen evidences of retardation of the 
stream; in other places, acceleration. These are phenomena that are not 
explicable on the basis of alterations of contractility of the arterioles. 

In certain of the acrocyanoses , Parrisius observed a remarkable series of 
contractions occurring in the arterial limbs of the capillary loops, together 
with atonic dilatation of the venous limbs. In one vein sudden interruptions 
of the column of blood could be seen in the venous limb of the capillary 
(Fig. 174). In his series of pictures the hiatuses are well depicted, and also 
the final fusion of the separated blood columns at /. Here is a beautiful 
example of spasm in the venous limb, gradually overcome either by pressure 
from the arterial side, or by relaxation of the spasm itself. And so we see 
that a spasm in the capillary territory can be responsible for interruption of 
the circulation. 

In short, under certain conditions, spontaneous activity is demonstrable 
in the capillary walls , which may result in an enhancement of the blood stream , 
or in its retardation . Although the capillaries are said by some to aid in the 
propulsion of the blood, Muller from his own observations cannot subscribe 
to the view that the capillaries of the body surface have either peristaltic or pulsa¬ 
tile activity of sufficient degree to be of functional value. He contends that 
it is only under special conditions, particularly with diminished vis a tergo 
and diseased states, that a tendency to contraction on the part of the capil¬ 
laries more regularly manifests itself. This view diverges radically from 
the hypothesis of Hooker, who, as elsewhere pointed out, ascribes a very 
important functional role to the capillaries in the mechanism of circulation. 


CHAPTER CVII 

CAPILLARY MICROSCOPY IN THE VASOMOTOR NEUROSES 

We have already made mention of the term, “ Vasoneurotic Constitution” 
or diathesis, as having been applied (Parrisius and Muller) to a certain vas¬ 
cular predisposition to excitation and have briefly discussed this in the 
chapter on Vasomotor Instability. Although this condition may become 
intensified by postnatal stresses, it is based on a constitutional status, and is 
but rarely purely acquired. It may affect both the motor and secretory func¬ 
tions of the capillary endothelium. And so we may recognize permanent 
deficiencies of function, divisible into 

1. Spastic or atonic complex of symptoms (motor); 

2. Secretory derangements of the capillary constituents. 

In the former, combinations or isolated manifestations of vasoconstrictor 
or vasodilator nature may predominate in the picture; in the latter the 
phenomena, such as edema and dystrophies, are to be expected. 

Capillary microscopy concerns itself especially with the former of these 
functional abnormalities. More recent observations on visual evidences 
of disturbed function in the realm of the capillaries and smallest arteries 
and veins will be the subject of discussion here, with illustrations from the 
excellent contributions of Muller. These have shown that data are forth¬ 
coming relative to 



CAPILLARY MICROSCOPY IN THE VASOMOTOR NEUROSES 591 

1. Spastic and atonic phenomena in the capillaries; 

2. Abnormalities of current and pressure; 

3. Abnormalities in morphology of the vessels; and 

4. Derangements of the permeability of the capillary wall. 

Nature of the Vasoneuroses. Continental medical thought seems to 
incline to the more general view of the nature of the vasoneuroses, and 
would regard these as partial manifestations of a concept— dysergia —or 
general constitutional anomaly. Such a diathesis—one of malfunction—is 
not regarded as purely somatic, but the result of the sum of psychic and 
vegetative forces. While we believe that the vegetative nervous system is 
quite independent of higher. centers, more and more evidences are forth¬ 
coming of the close interrelationship of the higher psychic activities, and the 
vegetative phenomena. And so, although there are cases in which mani¬ 
festations of dysergia seem to be limited to the vegetative nervous system 
and seem to be exhibited altogether in the form of derangements of vaso- 



Fig. 175.—Elongated, dilated and deformed capillaries of the subpapillary plexus in severe 
vasoneurosis at margin of nail. ( Muller) 

motility, careful investigat on will reveal that in most instances certain 
stigmata that would implicate the psyche of these afflicted individuals 
can be detected. 

We must recognize, therefore, that all do not admit of a justification for 
grouping the peripheral vascular affections as indicated in previous chapters. 
All do not concede the independence of such morbid complexes as Raynaud’s 
disease, acro-asphyxia and erythromelalgia. Indeed, if the concept of a 
combined neurodysergia, vegetative neurodysregia and psychic dysergia be 
accepted as the essential basis for the phenomena of disturbed vasomotility, 
then the various special diseases described in previous chapters would all be 
manifestations of this basic disorder. Valuable as this newer contribution 
to the interpretation of vegetative derangement may be, we are not yet able 
to relinquish altogether the discrete concepts previously described. We 
should adhere rather closely to the clinical forms as accepted by most clini¬ 
cians and relegate as nondescript manifestations all those other atypical 
phenomena of vasoneurosis that diverge from the time-honored clinical 
forms. The newer methods of capillary microscopy will enable us to recog¬ 
nize more clearly these latter types. 







592 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


i. Spasm and Atony of the Capillaries. —Capillary microscopy teaches 
us that not only do the vasomotor neuroses exhibit more or less continuous 
deviations in the form and size of the vascular lumina, but that contraction 
and dilatation may occur in variable sequence and often without apparent 
cause. Parrisius observed alternating spasm and atony of the capillaries 
in various types of vasoneurosis as well as in Raynaud’s disease (Fig. 175). 
Repeated observations will acquaint the observer with this remarkable 
occurrence of spasm and atony in the capillaries of the vasoneurotic patients. 
Sometimes a spastic condition will predominate, at others, atony. Even 
aneurysmal enlargements of the capillaries occur in these cases (Fig. 176). 
These deformities are not infrequently seen in so-called cases of acropares¬ 
thesia in which no explanation can be found for the pain and the sensory 
disturbances. 



Fig. 176.—Sac-like aneurysms of the capillaries in a severe case of vasoneurosis. ( MiiUer ) 

It has been latterly observed that a spastic or atonic condition of the 
capillaries, or even the larger vessels, may exist in young individuals to the 
degree of bringing about a condition of intermittent tonic spasm. Such a 
spasmophilic tendency may be associated (Kraus) with latent tetany; 
and the latter can be demonstrated by the Chvostek sign. With such arte¬ 
rial spasm there may be attendant dilatation of the cutaneous veins. 

Those authors who accept the hypothesis of a basic disturbance, both in 
the psychic and vegetative spheres as responsible for all types of vasomotor 
malfunction, regard the spastic or atonic symptom-complex as responsible 
for all the usual vasomotor phenomena. And so they consider the fugitive 
vasoconstrictor paresthesiae as only one form of the many transitions that 
lead into the complexes, erythromelalgia and Raynaud’s disease. But these 
affections are dependent upon disturbed motility of the vessels, and are 
distinctly separable from those in which there are evidences of derangement 
in the permeability of the vessel wall. 

2. Stream and Pressure Conditions in the Vasoneurotic Diathesis.— 
We must expect abnormalities in the flow through the capillaries when the 
latter are under either spastic or atonic influences. And so we see the blood 
course continuously and regularly, at other times rapidly, again retarded and 




CAPILLARY MICROSCOPY IN THE VASOMOTOR NEUROSES 593 


in granular fashion, or even brought to a standstill for a time. Or we may 
simultaneously see several of these variations in one microscopic field. 
Muller speaks of reflux from the venous into the arterial limbs of the capil- 



Fig. 177. —Giant loops with equally dilated venous and arterial limbs, in a case~of 
Raynaud’s disease, in stage of asphyxia. This figure shows a cyanotic capillary loop at the 
arrow, dilated loops to the right, interspersed with normal loops. ( Muller ) 



Fig. 178. —This figure demonstrates the vasoconstriction following subcutaneous 
injection of adrenalin solution (1 cc. of 1:1000) with consequent better delineation of 
the dilated capillaries, in capillaries depicted in Fig. 177. ( Muller ) 

laries, in vasoneuroses. Such a reversal is usually characteristic of insuffi¬ 
ciency of the circulation. Furthermore, observations of other^authors 







594 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


(Parrisius) depict how the capillaries and the blood color behave when 
stasis occurs. The external contour of the capillaries becomes irregular, and 
the accumulation of carbon dioxid gives the field a bluish or violet color. 
But even such dilated capillaries in the condition of atony may respond by 
some contraction upon the action of adrenalin (Figs. 177 and 178). Even 
the dilated capillaries in which stasis has taken place with marked cyanosis 
in cases of Raynaud’s disease have been shown to be able to undergo a certain 
amount of contraction. This is quite in accord with the observations of the 
author, who has demonstrated that the dilated capillaries of the lower 
extremities in thrombo-angiitis obliterans respond to dermatographic 
(mechanical) stimuli. 

Muller regards the abnormal vasomotility as occurring in capillary 
loops themselves and not consequent upon spasm in the arterioles and venules. 



Fig. 179. —Normal distribution of capillaries in the skin of the breast. ( Muller) 

He gives as a reason the observation, that if arteriolar spasm were responsible 
with diminished vis a tergo, two loops arising from one arteriole would be 
simultaneously affected, which is not the case; or, spasm of a subpapillary 
venule with consequent stasis cannot be given in explanation for a similar 
reason. 

Variations in papillary pressure are expressions of the abnormal lability 
of tension occurring in the vasoneuroses. Since the changes in capillary 
and arterial pressure do not go hand in hand, it is believed that alterations in 
the former may occur independent of the latter. 

In short, in the vasoneuroses and in vasoneurotic diathesis evidences of 
hyperirritability, hypo-irritability or asthenia, with concomitant manifesta¬ 
tions in flow and pressure are characteristic signs. 

Fullness of the Capillaries in the Vasoneurotic Diathesis .—Filling or over¬ 
filling of the capillaries may be a sign of the vasoneurotic status or may result 
from thermic or radio-active influences. In the vasoneuroses the papillary 
capillaries seem to be increased in number, the vessels are dilated, and there 



CAPILLARY MICROSCOPY IN THE VASOMOTOR NEUROSES 595 

seem to be more vessels in the subpapillary plexus. If we refer again to the 
observations of Krogh who emphasized the fact that normally a large number 
of capillaries are either partly or completely empty, we will understand that 
such vessels constitute a sort of reserve of the resting tissue or organ, capil¬ 
laries that can be sent into action for purposes of supply when occasion 
arises. In the case of the vasoneurotic individual that portion of the capillary 
territory which ordinarily is at rest, is also put into activity. And perhaps 
some of the peripheral as well as internal sensations are in part due 
to just this abnormal plenum in the capillary territory. A comparison of 
Fig. 180 with the normal in Fig. 179 will show that not only overfilling 



Fig. 180.—Elongated and dilated capillaries after 15 minutes’ exposure to sunlight; taken 
from skin of upper part of breast. ( Muller ) 

and multiplicity of capillaries are characteristic of vasoneuroses, but occa¬ 
sionally though more rarely, diminished supply of blood with pseudo-anemia 
has been observed. 

3. Morphology of Capillaries in Vasoneuroses. —Although of less impor¬ 
tance than the above described hyperirritability of the capillaries, the changes 
in morphology may be of some value in diagnosis. Acquired states depend¬ 
ing upon local conditions and more general influences must be taken into 
consideration, however. Thus, the nature of a person’s work may influence 
the state of the hands, and therefore the capillaries of the fingers; or excessive 
use of alcohol or other factors may cause deviations from the normal. Such 
must be excluded if the form of capillaries be interpreted for their diagnostic 
value. And furthermore, it is well to take the following into consideration 
(Muller) lest we over- or underestimate the significance of the morphology 
of capillaries: firstly, our data must be weighed in relation to other findings: 
secondly, repeated examinations in one or more places are required; and 
thirdly, artefacts must be excluded. 

With due consideration for the above, the capillary form and the vaso¬ 
neuroses will be seen to deviate as follows: the loops may be abnormally 



596 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


long or abnormally short; or, they may be abnormally dilated or constricted; 
or, their size may vary up to giant form, conserving either their normal 
axial relations or through unusual processes take on peculiar contours even 



Fig. 181.—Normal capillaries at margin of nail. ( Muller) 



Fig. 182.—Almost normal capillaries in mild vasoneurosis; possibly somewhat narrow and 

too long. ( Muller ) 

with extraordinary anastomoses. If we compare the normal capillaries 
(Fig. 181) with those depicted in Figs. 182 and 183, we will see the abnormal 
length as a characteristic change in vasoneurosis. Occasionally the capil¬ 
laries are abnormally small as depicted in Fig. 184. 



CAPILLARY MICROSCOPY IN THE VASOMOTOR NEUROSES 597 


Perhaps a more pathognomonic form of capillaries in vasoneurotic 
individuals is the type in which a large network of loops runs in sort of con¬ 
vergent or divergent form at the margin of the nail with dilatation of the 
venous limb, and possibly constriction of the arteriole (Fig. 185). 



u 

Fig. 183.—Elongated capillaries in mild vasoneurosis. ( Muller ) 


# n 
* * 

r fcr' 

• , • V . 

A 


* * 

v 

& 


* 

1 < 


j 


J > , 


s 


- 4. ■'[ 1 ‘ i ' ‘ >,<■ 


FlG . 184— Abnormally small capillaries in an adult neuropathic. ( Muller) 

4. Abnormalities of Permeability. —Unfortunately we are unable to 
visualize the interchange of fluids from the capillaries to the tissues, when no 
c’orpuscular elements are contained therein. Only blood can be seen passing 
through the capillary walls. This occasionally takes place in various forms 
of the vasoneuroses either spontaneously, or induced by trivial traumata. 





598 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


CHAPTER CVIII 

CAPILLARY MICROSCOPY IN SPECIAL FORMS OF 
VASOMOTOR DISEASE 

Acrocyanosis.—According to Erben 1 the cases may be divided into two 
types, firstly, those with pallid skin and prominent subcutaneous veins; 
and secondly, those with acrocyanosis and narrow subcutaneous veins. This 
author assumes that an atonic condition of the intracutaneous veins exists 
in this disease complex, with simultaneous spasm of the subcutaneous veins. 
In many of the cases relaxation of the subpapillary venous plexuses with 
simultaneous spasm of the arterial limb of the capillaries and the deeper 



Fig. 185.—Network of capillaries in a vasoneurotic individual. ( Muller) 


subcutaneous veins can be demonstrated by the “expression test.” This 
isj evidenced by a sluggish return from the periphery towards the center of 
theblanched area produced.by finger compression. Such circulatory 
return takes place after remission of pressure. This is a phenomenon not 
unlike that elicited by the compression or expression test previously described 
^ c ^ a P^ er on O r g a nic Arterial Diseases. With capillary microscopy 
the dilatation of the subpapillary plexus can be seen, but the arterial limbs 
are usually constricted. 

Erythromelalgia. In a case observed by Muller, the arterial limbs of 
the papillary capillaries were dilated, and the loops of the venous limb and the 
subpapillary plexus enlarged, even to a greater degree. In contradistinction 
to the phenomena m Raynaud’s disease, there is here an absence of the spasm 
of the arterial limb so characteristic of Raynaud’s. In erythromelalgia the 
atonic manifestations predominate. 

In some cases, however (Parrisius) the changes in form seem to be of a 
more permanent nature and cannot be attributed altogether to deviations in 
now through the capillaries (Fig. 186). 

1 Erben, Wien. klin. Wchnschr., 1918, Heft 2. 




CAPILLARY MICROSCOPY IN VASOMOTOR DISEASE 


599 


Raynaud’s Disease. —For an understanding of the circulatory phenomena 
in Raynaud’s disease, one must distinguish between a condition of pure stasis 
and one of ischemic stasis. In the latter the circulatory deficiency or arrest 
in the venous territory is due to spasm in the arterial limbs of the capillaries 
and diminished vis a tergo. In pure asphyctic conditions, however, there 
may be dilatation of both the arterial as well as the venous limbs of the 
capillaries, but between the dilated and relaxed saccules there may be normal 
loops functionating in a normal manner. Similar observations have been 
made by Halpert, who found side by side fine papillary capillaries with dilated 
giant loops. 

Between the attacks he observed granular streaming, only occasionally 
stasis. During the attacks all the loops showed stasis and a bluish or viola- 



Fig. i86 .—Giant loops in a case of erythromelalgia. ( Muller ) 

ceous discoloration, and only some of them showed a slow granular streaming. 
Besides this there were unusual processes noticeable in some capillaries; 
sometimes a slow peristaltic movement of the blood; at other times the latter 
retarded by spastic contraction. Warmth caused a paradoxical reaction in 
that the loops were occasionally narrowed with a concomitant acceleration 

of their blood flow. _ 

Fig. 187 is a beautiful example (Muller) of deformed capillaries in Ray¬ 
naud’s disease, with occasional hiatuses due to spasm; and Fig. 188 shows a 
giant capillary side bv side with a normal capillary. It is now believed that 
in Raynaud’s disease' severe general functional aberration may occur in the 
vascular system. The normal vascular reflexes to cold and warmth may be 
modified or altered. Niekau recently found abnormalities in the capillaries 
of the breast region, where the skin seems altogether normal. The capillaries 
and vessels of the subpapillary plexus in the upper breast region were found 

^Indeed, if these vascular changes were of considerable duration, secondary 
tissue changes might occur. By virtue of continued vascular spasm without 
evidences of gangrene or necrosis, atrophic skin with absent capillaries or 
very sparse distribution of these is observable. Spontaneous hemorrhages, 



600 


CIRCULATORY AFFECTIONS OF THE EXTREMITIES 


usually in the region of the connecting portion of the loop, are interesting 
and characteristic findings. 

In short, in the early stages of Raynaud’s disease capillary microscopy 
brings to light the existence of intensive degrees of spastic and atonic condi- 



Fig. 187.—Deformed capillaries in Raynaud’s disease with hiatuses due to spasm. ( Mul¬ 
ler) 




Fig. 188.—Normal and giant capillaries in same field (local asphyxia). ( Muller ) 

tions of the capillaries. Spasm and atony may occur simultaneously, or in 
sequence, or alternate. These functional abnormalities may implicate the 
arteries (even the larger ones) as well as the capillaries and veins. Although 
during the stage of syncope, spasm, not only arterial but capillary and 




CAPILLARY MICROSCOPY IN VASOMOTOR DISEASE 


601 


venous may occur, and during the asphyctic stage there is arterial and venous 
spasm, nevertheless one cannot speak of a regular or typical sequence of 
events in this disease. For, one can note the co-existence of spastic as well 
as atonic loops in one microscopic field. 

Erythromelia. —This subject has been discussed in detail in the chapters 
on Thrombo-angiitis Obliterans. Here we may call attention to the observa¬ 
tion that in the standing position the capillaries in the normal individual 
frequently show stasis. And it has been suggested that some of the fine 
capillary loops are in a state of contraction in order to facilitate the progress 
of the current through deeper and shorter circuits between arteries and veins. 
Krogh has emphasized the fact that normally all capillaries are not open 
simultaneously. The additional vasoconstriction in the standing position 
is also perhaps of teleological value in order to further the circulation. 
When erythromelia develops in this position, the normal vasoconstriction, 
as well as the normal emptiness of the capillaries must have given way to 
dilatation. And this occurs perhaps, because the need for such a spastic 
condition of the peripheral vessels is no longer present in the vascular obstruc¬ 
tive diseases. For, since the vis a tergo in the latter conditions is diminished, 
and the need for acceleration of blood for purposes of return is not so great, 
more capillaries are open than normally. Indeed, the whole capillary reserve 
becomes dilated and functionates. The rubor of organic arterial disease 
then simulates a neurotic papillary plenum, such as follows X-ray radiation, 
sunlight, or thermic (heat) influences. 

The grouping of erythromelia as a purely vasomotor, partly hydrostatic, 
or combined phenomenon, will depend upon one’s individual interpretation 
as to the dignity and importance of the mechanisms that bring it about. 































































































































































































































BIBLIOGRAPHIC INDEX 


Abadie, 524 

Achard and Demanche, 470 
Achard and Levi, 536 
Addison, 502 
Adrian, 567 

Allbutt, 63, 390, 402, 502 
Allan and Matas, 167 
Aschner, 495, 496 

Aschoff, 15, 19, 101, 105, 106, 107, 108, 
109, 114, 119, 126, 190, 192, 201, 395 
Aschoff and Welch, 124 
Askanazy, 123 
Audry and Constantin, 469 

Babes, 188 

Balzer and Vaudet-Neveux, 470 

Banting, 443 

Barbe, 469 

Bardy, 61 

Barker, 474 

Barker and Sladen, 528, 554 
Baruch and Kiittner, 524, 525 
Bauer, 494 

Baumel and Lardennois, 199 
Baumgarten, 108, 189 
Baumler, 456 

Bayliss, 25, 34, 37 , 38, 40, 55 

Bayliss and Gaskell, 34 

Belk, 452 

Benda, 121, 459 

Beneke, 103, hi, 122, 123, 124 

Bernard, 503 

Bernheim and Popsischill, 189 
Bessau and Pfeiffer, 191 
Bieling and Conradi, 192 
Bier, 54, 165, 195, 206, 507 
Bier and Specht, 198 
Bikeles, 533 
Bing, 46, 148, 152, 154 
Binkler, 564 

Bjerre and Cronequist, 567 
Boas, 63, 65, 67, 68 
Bolognesi, 83 

Bonardi and Chvostek, 529 

Bondesio, 469 

Bonnet and Gayet, 94 

Bordet, 103 

Borscher, 201 

Borst, 205 

Bother, 139 

Boullay, 139 

Bourgeois, 142, 157 

Boutelier and Thibierge, 566 

Braun, 212 


Breslauer, 518 
Breuer and Marburg, 511 
Brickner, 517 
Briggs, 184 

Briscoe, 40, 59, 60, 75, 76, 254 
Bronson, 567 
Bruce, 61 

Bruce and Meyer, 37 
Brugsch, 30 

1 Brugsch and Dresel, 56 
Brugsch, Dresel, and Lewy, 30 
i Brugsch, Kraus, and Dresel, 30, 38 
I Buchwald, 566 
I Buday, 189 

1 Buerger, 147, 149, 293, 308, 396, 397, 552, 
555 

Buerger and Heimann, 194 
Buerger and Kaliski, 277 
Buerger and Oppenheimer, 421 
Bundschuh, 180, 181 

Cannon, 61, 527 
Cannon and Dale, 62 
! Cardi and Castellino, 552, 553 
j Cassirer, 46, 47, 94, 95 , 97 , 9 8 , 99 , * 3 6 , 
141, 154, i 55 , 377 , 5 °°> 527 , 528, 53 °> 
53D 533, 538, 539 , 542, 545, 547 , 549 , 
552, 553 , 554 , 556 , 561, 562, 565, 567 , 

5 6 9 , . 

! Cassirer and Oppenheim, 140 
Castellino and Cardi, 552, 555 
Catiano, 177 

{ Charcot, 139, 140, 152, 1 57 
I Charcot and Hallion, 157 
Chiari, 191 

Chiari and Frohlich, 581 
Chipault, 478 
j Chodak, 485 
Chvostek and Bonardi, 529 
Cilimbaris, Coenen, and Thorn, 174 
Coenen, Lexer, Henle, and von Frisch, 168 
Coenen, Thorn and Cilimbaris, 174 
Collinot, 469 
Colmers, 170 
Comte and Hallion, 41 
Conradi and Bieling, 192 
Constantin and Audry, 469 
Continental School of investigators, 38 
Cotton, Slade and Lewis, 60 
Cramer, 545 
Crocq, 554 

Cronequist and Bjerre, 567 
Curschmann, 144 , 5°° 

| Cushing, 558 







604 


BIBLIOGRAPHIC INDEX 


Dale, 6i 

Dale and Cannon, 62 
Dale and Richards, 63 
Dale, Krogh, and Hooker, 508 
Danielsen, 213 

Danzer and Hooker, 61, 63, 66, 67, 68 
Dectjen, 106 
Dehio, 552 

Dejerine, 129, 146, 147 

de la Vergne and Sacquepee, 201 

Delbet, 524 

Demanche and Achard, 470 

Depisch, 510, 511 

de Rothschild and Levi, 545, 546 

Determann, 139, 146, 148, 153 

Dienst, 120, 124, 125 

Dieter and Weiss, 64, 65, 588 

Dietrich, 119 

Dieulafoy, 470 

Dinkier, 567 

Dogiel, 35, 46 

Donath, 574 

Dostre and Mathews, 105 

Doutrelepont, 567, 569 

Dresel, 30, 38, 43, 44, 501, 503, 581 

Dresel and Brugsch, 56 

Dresel and Lewy, 503 

Dresel, Brugsch and Lewy, 30 

Dresel, Kraus, and Brugsch, 30, 38 

Dreyer, 174 

Druelle, 458, 459, 461 

Dumont and Mosny, 494 

Dutil and Lamy, 152 

Eberth-Schimmelbusch, i 14 
Edinger, 41 

Eichorst and Mornet, 450 
Elsberg, 379 
Engelbach, 502 

Eppinger and Hess, 43, 501, 512 

Erben, 598 

Erichsen, 187 

Etienne and Lucien, 470 

Fahr, 70 

Farner and Klinger, 580 
Fessler, 200 
Ficker, 191, 196 
Finger, 469 
Fiolle, 524 
Fleisch, 52, 156 
Florcken, 173 

Flottes, Prat, and Violle, 185 
Foerster, 537 

Fontaine and Voivenel, 545 
Fontana, 478 
Foulerton, 561 
Fournier, 459 
Fournier and Loeper, 469 
Frankel, 192 
Franz, 194 
Frieboes, 464. 465 
Friederich, 484 
Friedlander, 152 
Friedmann, 538 
Frohlich and Chiari, 581 


Friind, 200 
Fuchs, 399 

Gaillard, 470 
Gartner and Strieker, 40 
Gaskell, 55 

i Gaskell and Bayliss, 34 
; Gayet and Bonnet, 94 
| Ghon and Sachs, 192 
Ginsberg, 381 
Girgolaf and Oppel, 545 
Girou, 523 
Glaser, 29, 35, 43 
Glaser and Muller, 35 
Goldflam, 141, 151, 152, 153 
Goldscheider, 46 
Goldstein and Parhon, 510 
Goubaux, 139 

Gouget and Roger, 449, 450, 495 

Grasset, 147 

Gross, 199 

Grossman, 139, 140 

Griinfeld, 186 

Guilera, 185 

Guillain and Rendu, 493 

Halpert, 67, 69, 599 
Hallion and Charcot, 157 
Hallion and Comte, 41 
Hamann, 51 
Hamilton, 535 
Hancken, 194 
i Hardy, 147, 561 
Harrop, Krogh, and Rehberg, 60 
Hartman, 56 
Hasebroek, 51 
Haskovec, 538 
Hayem, 117 
Head, 97, 483 
Heidrick, 210 
- Heitz, 583 

Heimann and Buerger, 194 

Heller and Lewin, 560, 562, 564, 565, 566 

Henius and Pribram, 67, 69 

Henle, 210 

Henle, Lexer, von Frisch, and Coenen, 168 

Henneberg, 514 

Hercher, 199 

Hering,. 79, 156 

Herxheimer, 566 

Hess, 125 

Hess and Eppinger, 43, 501, 512 

Heubner, 61, 396 

Heuzard, 469 

Heveroch, 574 

Hewlett, 76 

Higier, 139, 140, 144, 146, 149, 150, 152, 

153 , LS 4 , i 55 
{ Hinter, 567 
I Hintner, 569 
Hodara and Riehl, 173 
' Hodesmann, 194 
Hoesslin, 547, 558 

Hofmann, 70, 121, 467, 469, 475, 477 
Hoffmann and Kiister, 189 
Holmgren, 125 





BIBLIOGRAPHIC INDEX 


605 


Hooker, 52, 58, 59, 60, 61, 62, 507, 590 

Hooker and Danzer, 61, 63, 66, 67, 68 

Hooker, Krogh and Dale, 508 

Hopkins, 82, 156 

Horrax, 525 

Hoskins, 56 

Hotz, 85 

Hueck, 396 

Idelsohn, 152, 153, 154 
Isensch and Krehl, 28 
Ivens, 199 

Jacobsohn, 25 
Jacoby, 186 
Jaffe, 203 
Jansen, 123 
Johannessen, 212 
Johannsen, 484 

Jores, 15, 19, 20, 95, 395, 396, 398 

Josefson, 503 

Joseph, 567 

Joslin, 443 

Josue, 400 

Jungmann, 185 

Kahn, 154 

Kaliski and Buerger, 277 
Kamen, 196 
Kaposi, 569 

Karplus and Kreidl, 28, 44 
Klein, 521 

Klinger and Farner, 580 
Klose, 190, 203 
Klotz, 400, 463 
Klotz and Saltykow, 401 
Kobert, 186 
Kocher, 30 
Koga, 381 
Kohler, 154 

Kohlschiitter and Meyer, 174, 180 

Kollants, 554 

Kopp, 567 

Korte, 205 

Koyano, 277 

Kramer, 452, 454 

Kramer and Krumbhaar, 453 

Kraus, 30, 592 

Kraus, Brugsch, and Dresel, 30, 38 
Krause, 514 
Kravkof, 274 
Krehl and Isensch, 28 
Kreibich, 98, 567, 569 
Kreidl and Karplus, 28, 44 
Kretz, 127 ^ , , 

Krogh, 11, 38, 49 , 54 , 57 , 59 , 60, 61, 63, 75, 
502, 595, 601 

Krogh and Rehberg, 57, 5°9 
Krogh and Vimtrup, 58 
Krogh, Dale and Hooker, 508 
Krogh, Harrop, and Rehberg, 60 
Kroh, 180, 206, 514 
Krumbhaar and Kramer, 453 
Kiilbs, 400, 401 
Kussmaul and Maier, 462 
Klister, 104 


Kiister and Hoffmann, 189 
Kiittner, 171, 194 
Kiittner and Baruch, 524, 525 

Laewen, 588 
Lamb, 463 

Lamy and Dutil, 152 
Landois, 39 

Langley, 30, 35, 38, 39, 579 

Lapinsky, 95 

Lardennois, 199 

Lardennois and Baumel, 199 

Laveran, 152 

Lawson, 200 

Leclerc, 183 

Legros, 193 

Legroux, 560 

Lehman, 583 

Lehmann, 521 

Leichtenstern, 484 

Leloir, 567, 568 

Lenhossek, 93 

Lenmartz, 589 

Leriche, 36, 95, 99, 519, 522, 523, 524 
. 525, 559, 580, 581, 582, 583 
Leriche and Lyon, 98, 519 
Leriche and Pollicard, 69, 207 
Levai, 475 

Levi and Achard, 536 
Levi and de Rothschild, 545, 546 
Levy, 477, 478 
Lewandowsky, 40, 536 
Lewaschew, 39, 54 

Lewin and Heller, 560, 562, 564, 565, 566 
Lewis, Cotton and Slade, 60 
Lewy, 30 

Lewy and Dresel, 503 

Lewy, Brugsch, and Dresel, 30 

Lexer, Henle, von Frisch and Coenen, 168 

Libman, 369 

Libman and Strauss, 450 

Liepmann, 185 

Lilienthal, 382 

Linser,. 550 

Lobstein, 394 

Loeb, 120 

Loeper and Fournier, 469 

Loewi, 512 

Lombard, 63 

Long, 147 

Loven, 41 

Lowi, 580 

Lubarsch, in, 121, 126, 127 
Lucien and Etienne, 470 
Lyon and Leriche, 98, 519 

MacCallum and Vogtlein, 580 
Mackenzie, 46 
Mager, 510 
Magnus, 588 

Maier and Kussmaul, 462 
Mallory, 445, 446, 447 
Mandlebaum, 369 
Marburg and Breuer, 511 
Marburg and Ranzi, 514 
Marchand, 17, 177, 179 , 394 , 395 , 5*5 






606 


BIBLIOGRAPHIC INDEX 


Marchand, Orth and Weigert, 455 
Marinesco, 03, si? 

Marwedel, 194 
Matas, 51, 165, 166, 167 
Matas and Allan, 167 
Mathews and Dostre, 105 
Matzenauer, 187 
Mauss-Kruger, 519 
Mayer, n 
Mayesima, 537 
Mayesima-Koga, 277 
McCartney, Sladden, and McNee, 527 
McLean, 490 
McLeod, 443 

McNee, Sladden and McCartney, 527 
Melchior, 194 
Mendel, 126 
Menetrier, 456 
Mercier and Sieur, 199 
Mertz, 69 

Meyer, 278, 381, 384 
Meyer and Bruce, 37 
Meyer and Kohlschutter, 174, 180 
Mitchell, Weir, 97, 390, 531, 532, 533 
Mobius, 545 
Moleen, 536 
Monakow, 92, 94 
Monckeberg, 21, 491 
Monro, 545, 546, 548, 558 
Morat and Strieker, 37 
Moreau and Souques, 550 
Morgan, 533, 544 
Mornet and Eichorst, 450 
Mosenthin, 502 
Moskowicz, 165, 166, 167 
Mosny and Dumont, 494 
Muller, 28, 38, 40, 42, 45, 185, 390, 500, 
5i5, 567, 580, 584, 586, 589, 590, 593, 
594 , 595 , 598 , 599 
Muller and Glaser, 35 
Muller and Parrisius, 590 
Muller and Spalteholz, 585 
Muller and von Romberg, 500 
Muller and Weiss, 64, 584 
Murphy, 214, 494 

Nagelsbach, 53, 179 
Nasse, 187 
Nelaton, 474 
Neuberger, 568 
Neumann, 567 
Niekau, 584, 599 
Noesske, 181 

Nothnagel, 142, 148, 510, 537, 538, 539, 

542 , 553 , 554 
Novy, 192 

Nuttall and Welch, 193 

Oeconomakis, 529, 530 
Oppel, 274 

Oppel and Girgolaf, 545 
Oppenheim, 29, 138, 139, 140, 142, 143, 144, 
145,.146, 153, 256, 529, 533, 534 
Oppenheim and Cassirer, 140 
Oppenheim, Schlesinger and Remak, 513 
Oppenheimer and Buerger, 421 


J Orlowsky, 401 
Orth, 171, 484 

Orth, Marchand and Weigert,"455 
j Ortner, 146 
| Osborne, 545 
Osier, 117 

Pal, 70, 558 
Panas, 152 
Papadea 401 

Parhon and Goldstein, 510 
: Parrisius, 69, 571, 584, 590, 592, 594, 598 
Parrisius and Muller, 590 
Passini, 190 
Paul and Walton, 139 
Payr, 195 

Pearlman and Vincent, 70 
Pehu, 554 
Pelnar, 150 
j Perthes, 188, 189 
Pfeiffer and Bessau, 191 
Pibram, 565 
Pick, 163, 242, 566 
Pollicard and Leriche, 69, 207 
Ponselle and Ravaut, 465 
j Popsischill and Bernheim, 189 
Porta, 83 
Potts, 35 

Prat, Flottes and Violle, 185 
Pribram, 196, 559 
Pribram and Henius, 67, 69 
Proksch, 469 

Rademacher, 139 
Ranzi and Marburg, 514 
I Rasch, 503 

Ravaut and Ponselle, 465 
Ravaut and Thibierge, 470 
Rehberg and Krogh, 57, 509 
Rehberg, Krogh and Harrop, 60 
I Rekord, 147 

Remak, Schlesinger and Oppenheim, 513 
Renaut, 567 

Rendu and Guillain, 493 
Renshaw, 567 
Ribbert, no, m 
I Rich, 61 

j Richards and Dale, 63 
Riedel, 184 

Riehl and Hodara, 173 
Rischtler, 173 

Roger and Gouget, 449, 450, 493 
Rolleston, 484 

Rolleston, Weber, and Williams, 502 
Roques, 465, 468, 469 
Rosset, 457 
Rossolino, 29, 510 
Rouget, 11, 58, 60 
| Roussy, 469 
Rtilf, 144 
Rumpel, 194, 201 

Sabanajew, 494 
I Sabin, n, 35 
Sachs, 535 

I Sachs and Ghon. 192 




BIBLIOGRAPHIC INDEX 


607 


Sacquepee, 201 

Sacquepee and de la Vergne, 201 

Saltykow, 400, 401 

Saltykow and Klotz, 401 

Salzer, 205 

Samuel, 91 

Sartorius, 178 

Schade, 176 

Schaeffer, 94 

Schaffer, 56 

Schaumleber, 195 

Scheidemandel, 401 

Schenk, 489 

Schimmelbusch, 114, 188 

Schlesinger, 143, 256, 510, 513 

Schlesinger, Remak and Oppenheim, 5 

Schmidt, 452 

Schvene, 213 

Schultze, 553, 554 

Schulze, 537, 542 

Schum, 209 

Schwarz, 121, 470 

Seguin and Weinberg, 201 

Seiffert, 189 

Sencert, 210 

Seydel, 526 

Shaw, 535 

Sherrington, 44 

Sick, 203 

Sieur and Merrier, 199 
Silberstein, 191 
Silbert, 379 
Simon, 41, 142 
Singer, 567 
Sinkler, 567, 569 
Sippmann, 173 

Sladden, McNee, and McCartney, 527 
Slade, Cotton and Lewis, 60 
Sladen and Barker, 528, 554 
Solis-Cohen, 452, 545 
Sollier, 147 
Sommer, 139 

Sonnenburg and Tschmarke, 180 
Souques and Moreau, 550 
Sowles, 184 

Spalteholz and Muller, 585 

Specht and Bier, 198 

Starling, 29, 34, 36, 37, 52, 55 

Stauuing, 200 

Steel, 381 

Stein, 485 

Stetten, 382, 494 

Stewart, 50, 54, 56, 76, 80, 494 

Stich, 204, 210, 213 

Sticker, 175 

Stiefler and Volk, 174 

Strandberg, 470, 504 

Strasmann, 459 

Strauss, 383 

Strauss and Libman, 450 
Strieker and Gartner, 40 
Strieker and Morat, 37 
Strohmeyer, 181 
Strumpell, 570 
Sudeck, 95 
Sutter, 185 


| Talke, 119 
I Thandavaroyan, 184 
Thibierge, 561 

Thibierge and Boutelier, 566 
Thibierge and Ravaut, 470 
Thoma, 402 
Thomas, 279 

| Thorn, Coenen and Cilimbaris, 174 
Tinel, 522 
Tobias, 148 
Tomaselli, 478 
I Torok, 470 
Trachtenberg, 401 
Treves, 210 
j Truffi, 568, 569 
Tschmarke and Sonnenburg, 180 
J Tufher, 524 

Uschinski, 179 

Van Beuren, 199 
Vaudet-Neveux and Balzer, 470 
Vesigne, 474 
; Vimtrup, n 
Vimtrup and Krogh, 58 
Vincent, 56 

Vincent and Pearlman, 70 
Violle, Prat, and Flottes, 185 
Virchow, 395 

Virchow, von Recklinghausen and Zahn, 

Vogtlein and MacCallum, 580 
Voivenel and Fontaine, 545 
Volk and Stiefler, 174 
von Bardeleben, 119 

von Frisch, Lexer, Henle, and Coenen, 1,68 
von Haberer, 212, 213 
von Hibler, 191 
von Kries, 63 

von Manteuffel and Weiss, 307 

von Mosettig, 526 

von Recklinghausen, 179, 187, 515 

von Recklinghausen, Virchow and Zahn, 117 

von Romberg, 390 

von Romberg and Muller, 500 

von Stapelmohr, 184 

von Winiwater, 174, 179, 307 

Votsch, 139 

Walton, 140 
Walton and Paul, 139 
Wassermann, 196 
Wachtel, 181 

Weber, Rolleston and Williams, 502 
Wedensky, 148 

Weigert, Orth, and Marchand, 455 
Weinberg and Seguin, 201 
Weir Mitchell, 97, 390, 531, 532, 533 
Weiss, S3, 68 , 547, 55 °, 5 ^ 4 , 588 
Weiss and Dieter, 64, 65, 588 
Weiss and Muller, 64, 584 
Weiss and von Manteuffel, 307 
Welch, 192, 193 
Welch and Aschoff, 124 
Welch and Nuttall, 193 
Weljamowitz, 469 
Welsh, 125 





608 


BIBLIOGRAPHIC INDEX 


Westphal, 143, 256, 550 
Wiesel, 454 

Wieting, 177, 179, 181, 194, 382, 526 

Williams, Weber and Rolleston, 502 

Wilonski, 307 

Wilson, 502 

Wolf, 381 

Wolff, 210, 212 

Wormser, 449 


Zahn, iii, 117, 123 

Zahn, von Recklinghausen and Zahn, 

Zak, 45, 155, 507 

Zenker, 104 

Zeiss, 586 

Ziegler, 401 

Zieler, 567, 570 

Zuckerkandl, 174 

Zurhelle, 278 



INDEX OF SUBJECTS 


Abscheidung’s thrombus, ioi 
Absence of pulsation distal to occlusive 
thrombi, 134 
in gangrene, 129 
Accretion thrombus, no 
Acid, lactic, effect of, on blood vessels, 54 
Acroasphyxia, acromegaly and, 529 
chronic, 527 
diagnosis, 530 

Raynaud’s disease and, differentiation, 
554 

hypertrophica with marked trophic 
changes, 528 

in cardiac irritability, capillary pressure 
in, 76 

Acrocyanosis, 75 

capillary microscopy in, 598 
capillaries in, 66, 68 
chronica anaesthetica, 528 
diagnosis, 530 

in Raynaud’s disease, 71, 7 2 
thyroid therapy in, 503 
Acromegaly, acroasphyxia and, 529 
gigantism and, 530 
Acromicria, 563 
Acroparesthesise, 537, 592 
analysis of symptoms, 538 
clinical course, 538 
objective sensations, 538 
of Schultze, Raynaud’s disease and, differ¬ 
entiation, SS3 
pathogenesis, 539 
prognosis, 539 
treatment, 539 
vasomotor symptoms, 538 
Actinic influences, thrombosis due to, 123 
irritants, cutaneous responses to, 509 
Acute arteritis, 448; see also Arteritis, acute. 
Addison’s disease, adrenalin in, 70 
Adrenalin as vasoconstrictor, 72 

effect of, on sympathetic nervous sys¬ 
tem, 580 

on vegetative functions, 512 
nervous system, 55 
in Addison’s disease, 70 
injections in experimental arteriosclero¬ 
sis, 400 . 

with glucose solution, injection 01, 
gangrene following, 185 
Adrenin, effect of, on bloodvessel tonus, 55 
Agglutination in thrombus formation, 102 
process of, 102 
Air embolus, 205 

hot, treatment, in arteriosclerosis, 437 . 
Akinesia algera, intermittent claudication 
and, differential diagnosis, 157 


Alcohol as causal factor in atherosclerosis, 
22 

Amputation, spontaneous, in gangrene, 159 
Anaerobic bacilli, 192 
sepsis, 196 

Anastomosis, arteriovenous, in treatment 
of thrombo-angiitis obliterans, 382 
circumpatellar, 86 
normal, 10 

Anatomical considerations, 3 
Anatomy, recent views on, 30 
Anemia, local, 71 
causes, 71 

diminished arterial influx in, 72 
mechanical diminution of patency of 
arteries in, 72 
neuro-irritative, 72 

obstructive, vasoconstriction and vaso¬ 
dilatation as sequences, 74 
spastic, 72 

Anemic territory, r 61 e of chemicals in, 156 
Aneurysm, aortic, and embolism, 493 
false, 208 

circumscribed, 209 
diffuse, 209 
Aneurysms, 208 

circulatory symptoms, 209 
complications, 209 
false, 208 

gangrene complicating, 209 

ligation and treatment of, 211 

pseudo-, 208 

symptoms, 209 

traumatic, 208 

treatment of, 211 

true, 208 

Angina cruris, 140 . 

Angioneurotic intermittent claudication 
with Raynaud’s disease of finger, 144 
Angiosklerotische intermittierende Muskel- 
parese, 140 

paroxysmal myasthenia, 140 
Angiospasm, cause of, theories of, 156 
relation of, to organic type of intermittent 
claudication, 144 
Angiospastic gangrene, 544 
Angle of circulatory sufficiency, 163 
Antagonistic innervation of vessels, 34, 40 
Antidromic impulses, 37 
Antithrombin, 104 . 

Antitoxin and toxin formation in gas gan¬ 
grene, 190 

Aorta, bifurcation of, embolism at, 486 
Aortic aneurysm and embolism, 493 # 

Aortitis, acute, embolism and thrombosis 
in, 493 


39 









610 


INDEX OF SUBJECTS 


Apokamnosis, 151 

Apparatus for visualization of capillaries, 
586 

Arocyanosis, cyanosis resembling, 577 
Arsenic as cause of gangrene, 183 
Arsphenamin, injection of, gangrene of 
fingers due to, 185 

Arterial diseases, organic, Raynaud’s dis¬ 
ease and, differentiation, 557 
vasoneurosis and, 578 
hyperemia, 73 

hypotension, endocrine disease in, 502 
obturation without immediate symptoms, 
480 

pulsation as diagnostic symptom, 132 
in Raynaud’s disease, 550 
in thrombo-angiitis obliterans, 263; 
see also Thrombo-angiitis obliterans , 
arterial pulsation in. 
spasm, 77 

thrombosis with traumatic gangrene, 170 
Arteries, anatomy, 13 

blood delivered by, and pressure in, 
factors influencing, 48 
development of, and subsequent path¬ 
ological changes, 21 
hypertrophy of, 447 

in embryonal development, elastic type, 

13 

muscular type, 14 
structure of, 13 

in extrauterine development, 15 
elastic type, 15 
muscular type, 15 

large, neurovascular syndromes after 
ligation of, 212 

larger, relation of, to nutrition of part, 
210 

lesions due to disturbances of growth 
and development, 445 
to disturbed nutrition, 445 
to infectious lesions, 446 
to special infectious agents, 447 
to toxic effects, 446 
miscellaneous affections of, 445 
pathology, 445 

sclerotic, bone formation in, 421 
senile changes in, 19 
shortly before birth, 15 
tuberculosis of, 455 
Arterioles, anatomy, 12 
Arteriorrhaphy, 212 

Arteriosclerosis associated with thrombo¬ 
angiitis obliterans, 306 
chemical action in, 82 
clinical course, 392 
manifestations, 385 
diagnosis, 431 

embolism and thrombosis complicating, 
493 

erythromelia of upper extremities in, 389 
experimental, 400 

human and, relation of, 401 
localization of, 401 
minute pathology, 402 
in calcification, 420 


Arteriosclerosis, minute pathology, intima 
in larger vessels, 416 
larger arteries in gangrene, 407 
media in obliterated arteries, 411 
lesions when lumen is filled, 413 
mixed occlusion, 415 
occlusive process in, 415 
of smaller vessels, 418 
recent occlusion of atherosclerotic 
popliteal artery, 411 

of lower extremities, clinical forms of, 385 
of trophic disturbances and 
gangrene in, 393 
special symptoms, 389 
trophic disturbances and gangrene 
in, 390 

pathogenesis, 394 

pathology, elastic fibers in normal arteries, 

396 

hyperplastic intima in, 398 
Jores’s theories of, 398 
peripheral, 71 

precocious development of, 22 
prognosis, 434 

simulating thrombo-angiitis obliterans, 
431 

treatment, 435 

according to case types, 438 
amputation, 440 
Buerger’s postural, 436 
diathermic, 438 
hot air, 437 " 

methods of improving circulation, 436 
of gangrene with hyperglycemia, 442 
without hyperglycemia, 442 
of trophic disorders and gangrene, 438 
postural, Buerger’s method, 436 l 
surgical, 443 

cases with hyperglycemia, 444 
without hyperglycemia, 444 
vascular insufficiency in, 71 
vasomotor phenomena in, 390 
with calcification, minute pathology, 420 
with mixed occlusion, minute pathology, 
420 

with thrombosis, atrophy as sequel, 425 
clinical course, 421 

diagnosticated as acute intermittent 
claudication, 150 
of larger more central paths, 424 s1 
gangrene with diabetes, 427 

complicating infection, 428 
pathology, 427 
with thrombosis, 421 
clinical history, 422 

Arteriovenous anastomosis in treatment 
of thrombo-angiitis obliterans, 382 
Arteritis, acute, 448 
etiology, 449 
of unknown origin, 452 
pathogenesis, 454 
pathology, 449 
symptomatology, 450 
elastica, 307 
migrating, 305 
parietal, 451 





INDEX OF SUBJECTS 


611 


Arteritis, rheumatic, 451 

syphilitic, and gangrene, 456 
clinical forms, 460 
incidence, 459 
pathology, 456 
symptomatology, 460 
with thrombosis simulating thrombo¬ 
angiitis obliterans, 454 
Artery, axillary, anatomy, 3 
brachial, anatomy, 5 
dorsalis pedis, anatomy, 10 
femoral, anatomy, 6 

common, nerve distribution about, 36 
popliteal, anatomy, 7 

palpation of, Buerger’s method, 133 
radial, anatomy, 5, 6 
tibial, anterior, anatomy, 10 
posterior, anatomy, 9 

and vein, normal, characteristics, 18 
ulnar, anatomy, 5, 6 
Artificial intermittent claudication, 151 
pallor, 151 

Aschoff gas edema bacillus, 191 
Asphyxia, localized, with arteries pulsating, 
572 

of fingers, hands, and feet, 75 
of irritable hearts, 75 

Asphyxie locale et gangrene symmetrique 
des extremit6s, 544 
Asthma, 503 

Atheroma, thrombus formation in, 121 
Atherosclerosis; see Arteriosclerosis. 

Atony and spasm of capillaries, 592 . 
Atrophy as sequel to arteriosclerosis with 
thrombosis, 425 
of skin, idiopathic, 566 
secondary, of nervous system, 94 
Atropin, effect of, on vegetative functions, 
5i3 

Atypical vasomotor neuroses, 572 
Autonomic action of capillaries, 58 
and vasomotor responses, 53 
nervous system, 23 
Axillary artery, anatomy, 3 
pulse, 5 
vein, 5 

Axon reflexes, 37 

Babinski-Froment type of reflex con¬ 
tractures, role of sympathetic in, 582, 583 
Bacillus aerogenes capsulatus, 190 
anaerobic, 192 
Frankel, gas, 190 
gas, 190 

Ghon-Sachs, 192 

of malignant edema, 191 

paratyphus, 203 

paredema, Pfeiffer-Bessau, 191 

Pfeiffer-Bessau, 191 

phlegmones emphysematosae, 190 

von Hibler, 191 

Welch, gas, 190 

Bacteria and thrombus formation, 120 
pyogenic, gangrene due to, 202 
Baths, hot, action of, on vascular tonus, 
70 


Bees and wasps, poison of, gangrene from, 

A 8 3 

Bifurcation of aorta, embolism at, 486 
Birth, arteries shortly before, 15 
Blanched condition of extremity in gan¬ 
grene, 129 
| Blanching, 73 

i Blood, color of, in acrocyanosis, 75 
flow in capillaries, 66 

in extremities, measure of, 49 
measuring, Stewart’s method, 50 
normal, in capillaries, 586 
movement, bloodvessels and, 51 
capillary circulation and, 52 
pressure, capillary, estimation of, 67 
Blood vessel tonus, effect of adrenin on, 56 
Blood vessels, blood movement and, 51 
chemical regulation of, 54 
effect of metabolites on, 54 
in gas gangrene, 193 
injuries to, and gangrene, 204 
arteriorrhaphy in, 212 
complications, 206 
control of hemorrhage, 209 
permanent, 210 
due to treatment, 204 
ligation and treatment of aneurysms 
in, 211 

nerve injury complicating, 206 
of main artery or vein, 207 
pathology, 204 
recent, 204 
results of, 205 

relation of larger arteries to nutrition 
of part, 210 

surgical treatment, principles under¬ 
lying, 211 
treatment, 209 

control of hemorrhage, 209 
permanent, 210 

role of, in thermic gangrene, 177 
trophic influences of nerves on, 95 
Bluish discoloration in gangrene, 129 
| Blushing, 73, 505 

I Bodies, solid, thrombosis due to, 122 
Boiterie intermittente des chevaux, 140 
Bone formation in sclerotic arteries, 421 
Borderline cases, 575 

cyanosis resembling arocyanosis, 577 
developing ischemia, probably 
thrombo-angiitis, 577 
early thrombo-angiitis obliterans, 576 
incipient thrombo-angiitis obliterans 
with apparent vasomotor symptoms, 
576 

varieties, 575 

vasoneurosis and organic arterial dis¬ 
ease, 578 

with cyanosis of toes as chief symp¬ 
tom, 577 . , . . . 

with limited asphyxia and with pam, 
578 

Brachial, artery, anatomy, 5 
pulse, 5 

Bronze erysipelas, 190 

Brown-Sequard theory of tropic disorders, 91 






612 


INDEX OF SUBJECTS 


Buerger’s method of palpating popliteal 
artery, 133 

postural treatment, 77 
Bullet wounds of peripheral nerves, vaso¬ 
motor and trophic symptoms fol¬ 
lowing, 520 

spasm of vasoconstrictors following, 
206 

Burns, thrombosis after, 119 

Calcium chloride in circumscribed edemas, 
78 

effect of, on sympathetic system, 581 
metabolism, altered, in spasmophilic 
conditions, 580 

salts, role of, in spasmophilic tendency, 79 
Cancer aquaticus, 188 
Cancrum oris, 188 

Capillaries, abnormalities of permeability 
of, 597 
anatomy, 11 
autonomic action of, 58 
blood flow in, 66 
contractile cells of, 12 
dilatation of, following action of cold, 53 
direct response of, to chemical stimuli, 60 
to mechanical stimuli, 60 
endothelial layer of, 11 
fullness of, in vasoneurotic diathesis, 594 
function of, summary of, 61 
granular streaming in, 586 
in acrocyanosis, 66, 68 
in vasoneuroses, morphology of, 595 
minute structure of, 11 
morphology of, 65 
muscular coat of, n 
nerves of, 11 
normal flow in, 586 

papillary, contractile phenomena in, 
588, 589 

paralytic action of poisons on, 61 
physiology of, 57 
spasm and atony of, 592 
spasms of, in Raynaud’s disease, 67 
vascular, intermittent spasm of, 144 
visualization of, apparatus, 586 
Capillary activity and capillary stream, 588 
blood pressure, estimation of, 67 
circulation and blood movement, 52 
derangement of, 76 
general considerations, 57 
in closed vascular territory, Weiss 
and Dieter’s studies, 64 
Lombard’s method of studying, 63 
methods of investigating, 63 
results of tests, 68 
nerve control of, 59 
spasm in, 589 
stases in, 589 
variations in, 64 

Weiss-Mtiller method of studying, 64 
microscopy, 584 

anatomical considerations in, 584 
in acrocyanosis, 598 
in erythromelalgia, 598 
in erythromelia, 601 


Capillary microscopy in Raynaud’s disease, 
599 

in special forms of vasomotor dis¬ 
ease, 598 

microscopy in vasomotor neuroses, 590 
abnormalities of permeability in, 
597 

morphology of capillaries in, 595 
nature of vasoneuroses in, 591 
spasm and atony of capillaries 
in, 592 

stream and pressure conditions 
in vasoneurotic diathesis, 592 
Muller’s Zeiss apparatus for, 587 
motility, nerve influences in, 38 
stream and capillary activity, 588 
Carbolic acid gangrene, 183 
Carbon dioxid, effect of, on blood vessels, 
54 

monoxid gangrene from, 184 
Cardiac disease, embolic gangrene with, 485 
weakness as factor in thrombosis, 123 
Causalgia, sympathetic nerves in relation 
to, 522 

nervous system and, 583 
Cellifugal degeneration of nervous sys¬ 
tem, 92 

Centers, cerebral vasomotor, 28 
subcortical vasomotor, 30 
vascular nerve, 44 
vasomotor, physiology of, 41 
spinal, 31 

Central nervous system, vasomotor and 
trophic disturbances in lesions of, 513 
Cerebral lesions of vegetative nervous 
system, localization of, 510 
vasomotor centers, 28 
Charcot-Erb type of intermittent claudica¬ 
tion, 140 

Chemical regulation of blood vessels, 54 
stimuli, direct response of capillaries to, 60 
Chemicals, gangrene due to, 181; see also 
Gangrene due to chemicals and drugs. 
role of, in an anemic territory, 156 
| Chilblain, 173 

Chorea, embolic gangrene complicating, 485 
Chromic acid as cause of gangrene, 182 
Circulation, capillary, and blood move¬ 
ment, 52 

general considerations, 57 
in closed vascular territory, Weiss and 
Dieter’s studies, 64 
Lombard’s method of studying, 63 
methods of investigating, 63 
results of tests, 68 
nerve control of, 59 
spasm in, 589 
stasis in, 589 
variations in, 64 

Weiss-M tiller method of studying, 64 
collateral, 82 

course of new channels in, 84 
demonstration of collaterals in obstruc¬ 
tive vascular disease, 84 
Mosckowicz test for investigation of, 210 
when peripheral arteries are patent, 85 




INDEX OF SUBJECTS 


613 


Circulation, effect of adrenalin on, 56 
of histamin on, 61 
of hypophysis cerebri on, 56 
of pituitrin on, 56 

general, under pathological conditions, 69 
Henle-Coenen test for, 168 
impaired, symptoms of, in gangrene, 128 
in extremities under pathological con¬ 
ditions, clinical manifestations, 87 
internal secretions and, 55 
ischemia an index of, 242 
local, pathological, 71 
Matas test for, 166 

methods of improving, in arteriosclero¬ 
sis, 436 

Moskowicz test for, 166 
peripheral, elementary principles, 48 
functional disturbances of, 76 

derangement of capillary flow 
in, 76 

due to impaired exchange of 
fluids, 78 

functional derangement of lym¬ 
phatic system in, 79 
physiology of, 48 

superficial, in obstructive vascular dis¬ 
eases, 80 

changes in vasomotor mech¬ 
anism in, 81 

chemical action on tissues in, 81 
diminished force of stream in, 80 
exhaustion in, 81 
hydrostatic and gravity forces 
in, 80 

tests for, 165 

value of, in thrombo-angiitis oblit¬ 
erans, 167 

vasomotor function and, 52 
Circulatory disturbances in blood vessel 
injuries, 206 

neuroses, vasomotor, Raynaud’s disease 
and, differentiation, 554 
sufficiency, angle of, 163 
Circumpatellar anastomosis, 86 
Circumscribed edema, 96 
calcium chloride in, 78 
false aneurysm, 209 

Claudication, intermittent, acute forms, 148 
age incidence, 152 

angioneurotic, with Raynaud’s dis¬ 
ease of finger, 144 

angiospasm in, theories as to cause, 156 
artificial, 151 

as diagnostic symptom, 137 
Charcot-Erb type, 140 
circulatory and vasomotor phenomena 
in, 141 

clinical course, 142 
clinical types, 140 
critical summary, 154 
differential diagnosis, 157 
Erb type, characteristics, 137 
examination of pedal and crural ar¬ 
teries, 142 

explanation of phenomena in, 155 
functional vasomotor type, 142 


! Claudication, intermittent, historical, 139 
in gangrene, 129 
in other territories, 146 
of inactivity, 136 
of spinal column, 146 
of upper extremities, 147 
of vasomotor type, 138 
organic type, relation of angiospasm 
to, 144 

par obliteration arterielle, 140 
pathology, 151 

Raynaud’s syndrome and, differentia¬ 
tion, 138 

sex and race incidence, 153 
tobacco as etiologic factor in, 153 
type accompanying organic vascular 
disease, 139 

with healthy arteries, 155 
j Clinically borderline cases, 575 
varieties, 575 

j Closed circuit and nerve impulses, 91 
Coagulation, extravascular, 102 
fibrin, 103 

in process of thrombosis, 108 
in thrombus formation, 102 
thrombosis, 101 
primary, 108 

Cold as vasoconstrictor, 72 
dry, effect of, on human tissues, 172 
effect of, on human tissues, 172 
local changes due to, first degree, 173 
second degree, 173 
third degree, 174 
neuralgia due to, 174 
reflex response to, 72, 76 
wet, effect of, on human tissues, 173 
! Coldness in thrombo-angiitis obliterans, 261 
of extremity in gangrene, 129 
Collateral avenues, 83 
circulation, 82 

course of new channels, 84 
demonstration of collaterals in obstruc¬ 
tive vascular disease, 84 
Mosckowicz test for investigation of, 
210 

when peripheral arteries are patent, 85 
hyperemia, 82 

j Collaterals in obstructive vascular disease, 
demonstration of, 84 
therapeutic development of, 87 
when peripheral arteries are patent, 85 
Colliquation necrosis, 183 
1 Communicating hematoma, 208 
Compression test, 77 
j Congelation, 100 

in thrombus formation, 105 
Conglutination, 100 
thrombosis, 101 

I Constitution, vasoneurotic, 572 
Contracture, ischemic, of muscles, without 
gangrene, in blood vessel injury, 206 
l Contractures at elbow, sympathetic in its 
relation to, 582 
Core, 127 

j Corpus striatum, nuclei in, 31 
Crises, vascular, 70 




G14 


INDEX OF SUBJECTS 


Cutaneous responses to thermic and 
actinic irritants, 509 
Cyanosis and rubor, 573 
in gangrene, 129 

in thrombo-angiitis obliterans, 250; see 
also Thrombo-angiitis obliterans , cyano¬ 
sis in , 250 

of fingers, hands, and feet, 75 
resembling arocyanosis, 577 
Cytozym, 103 

Danzer and Hooker’s method for capillary 
blood pressure estimation, 67 
Death, eczema, 504 
molecular, 127 
tissue, signs of, 128 
Decollement, 169 
Decubitus, 160 
acute, 97 

acute traumatic, 170 
after spinal cord lesions, 514 
Defense musculaire, 45 
Degeneration, indirect, of nervous system, 
94 

Lenhossek cellifugal, of nervous system, 
9 2 

nerve, interdependence of portions of 
nervous system in, 92 
retrograde, of nervous system, 93 
Wallerian, of nervous system, 92 
Demarcation, line of, in gangrene, 159 
Dermatographia, 60, 247 
rubra, 247 

Dermatoscleroses, 559 
Diabetes, endocrine glands in, 503 
with arteriosclerotic gangrene, 427 
Diabetic gangrene, 427 
Diagnostic symptoms, 132 
arterial pulsation, 132 
intermittent claudication, 137 
pain, 135 
Diapedesis, 77 
causes, 79 

endothelial symptom in, 80 
individual susceptibility to, 80 
postanemic, 77 
Diathesis, vasoneurotic, 590 

fullness of capillaries in, 594 
stream and pressure conditions in, 592 
Dieter and Weiss’s] method of studying 
capillary circulation, 64 
Diffuse false aneurysm, 209 
Dilatation of capillaries following action 
of cold, S3 

Diphtheria, gangrene with, 484 
Diphtheritic form of hospital gangrene, 
188 

Direct response of capillaries to chemical 
stimuli, 60 

to mechanical stimuli, 60 
Discoloration, bluish, in gangrene, 129 
Diseases, general, thrombosis_and, i23 
Distant thrombosis, 109 
Doigt mort, 72 

Dorsalis pedis artery, anatomy, 10 
pulse, 10 


Drugs, action of, on sympathetic nervous 
system, 580 

gangrene due to, 181; see also Gangren 
due to chemicals and drugs. 

Dry gangrene, 157, 158, 391 

of one or more phalanges, 202 
Dysbasia angiosclerotica, 145, 389 
intermittens, 140 

neurasthenica, intermittent claudication 
and, differential diagnosis, 157 
Dysergia, 591 

Dyskinesia intermittens angiosclerotica, 148 
Dyspragia intermittens angiosclerotica in- 
testinalis, 146 

Eclampsia, tendency to thrombosis in, 119 
Eczema death, 504 
Edema, 79 

circumscribed, 96 

calcium chloride in, 78 
evanescent, 78 
fugax, 79 
gas, 190, 197 

bacillus, Aschoff, 191 
inflammatory, 79 
malignant, bacillus of, 191 
war, 70 

Elbow, contractures at, sympathetic in its 
relation to, 583 
Emboli, infectious, 479 
Embolic and thrombotic gangrene after 
infectious diseases, 481 
clinical course, 481 
pathology, 483 
types of gangrene, 483 
arteriotomy in, 494 
technic, 498 

arteriovenous anastomosis in, 494 
diagnosis, 489 
embolectomy in, 494 
technic, 498 
ligation in, 494 
post-operative, 489 
treatment of, 493 
gangrene complicating chorea, 485 
with cardiac disease, 485 
Embolism and thrombosis, 479 

arterial obturation without immediate 
symptoms, 480 
classification, 479 
complicating arteriosclerosis, 493 
in acute aortitis, 493 
at bifurcation of aorta, 486 
in gangrene, 161 
without gangrene, 480 
Embolus, air, 205 

Embryonal development, structure of 
arteries in, 13 

Emotions, intensive, effects of, 513 
Emphysematous gangrene, 190 
Endarteritis obliterans, 214, 307 
tuberculous, 456 

Endocrine glands and functions of vegeta¬ 
tive nervous system, 502 
relation of, to vegetative nervous 
system, 55 






INDEX OF SUBJECTS 


615 


Endogenous poisons in thrombosis, 119 
Endothelial symptom, 80 
Epidermolysis bullosa hereditaria, 550 
Epilepsy, Jacksonian, vasomotor, 29 
Erb-Charcot type of intermittent claudica¬ 
tion, 140 

characteristics, 137 
Erb’s syndrome, 129 
Ergot as cause of gangrene, 181, 186 
Ergotism, 72, 186 
Ergotoxin as vasoconstrictor, 72 

effect of, on sympathetic nervous system, 
580 

gangrene from, 186 
Erkaltungsneuralgie, 174 
Erysipelas, bronze, 190 
Erythema, 523 

nodosum, differential diagnosis, 469 
Erythemata of nervous origin, 74 
Erythromelalgia, 216, 531 
associated symptoms, 532 
capillary microscopy in, 598 
clinical course, 534 
coexisting maladies, 533 
diagnosis, 534 
extent of rubor in, 532 
Foerster operation in, 537 
hyperesthesia in, 532 
local motor disorders in, 533 
pain in, 135, 531 
pathogenesis, 533 
prognosis, 534 

Raynaud’s disease and, differential diag¬ 
nosis, 553 

redness and swelling in, 532 
secretory disturbances in, 532 
sensory disturbances in, 533 
syndrome of, 534 

thrombo-angiitis obliterans and, differ¬ 
ential diagnosis, 534 
treatment, 536 
trophic lesions in, 533 
Erythromelia, 74, 89, 129, 163 
capillary microscopy in, 601 
chronic, 163 

in thrombo- angiitis obliterans, 242; see 
also Thrombo-angiitis obliterans, ery¬ 
thromelia in. 

of lower extremities, 390 

of upper extremities in arteriosclerosis, 

389 

Erythromelie, 242, 566 
Evanescent edema, 78 
Exercise of neurotrophic influences, 91 
Exogenous poisons and infectious agents, 
action of, in thrombus formation, 
120 

in thrombosis, 120 
Expression test, 163 

Extrauterine development, arteries in, 15 
Extravascular coagulation, 102 
Extremities and trunk, vasomotor paths of, 
5 11 

blood flow in, measure of, 49 
circulation in, under pathological condi¬ 
tions, clinical manifestations, 87 


Extremities, lower, arteriosclerotic disease 
of, clinical forms of, 385 
erythromelia of, 390 
in arteriosclerosis, 389 
intermittent claudication of, 147 
involvement of, in thrombo-angiitis 
obliterans, 294 

Extremity, coldness of, in gangrene, 129 

Facial blush, 73 
hemi-atrophy, progressive, 91 
False aneurysm, 208 
circumscribed, 209 
diffuse, 209 
Feet, asphyxia of, 75 
cyanosis of, 75 

Females, thrombo-angiitis obliterans in, 226 
Femoral artery, anatomy, 6 

common, nerve distribution about, 36 
pulse, 7 

vein, ligation of, in treatment of thrombo¬ 
angiitis obliterans, 382 
Fibrin coagulation, 103 
Fibrinogen, source and quantity of, 105 
Fibrinolysis, 104 
Fingers, asphyxia of, 75 
cyanosis of, 75 

gangrene of, due to injection of arsphen- 
amin, 185 

Fissures on feet, in thrombo-angiitis 
obliterans, 236 

Focal migrating phlebitis of unknown 
origin, 470, 472 

Foerster operation in erythromelalgia, 537 
Formalin as cause of gangrene, 182 
Frankel gas bacillus, 190 
Freezing, effect of, in thermic gangrene, 176 
local, first degree, 173 
. second degree, 173 
symptomatology of, 173 
third degree, 174 

thrombosis as cause of gangrene after, 
179 

treatment, 180 
Fugitive edema, 79 

Functional vasomotor type of intermittent 
claudication, 142 

Gangrene, absence of pulsation in, 129 
and syphilitic arteritis, 456 
clinical forms, 460 
incidence, 459 
pathology, 456 
symptomatology, 460 
and trophic disturbances in arterio¬ 
sclerotic disease, 39 
clinical forms of, 393 
angiospastic, 544 

arteriosclerotic, with diabetes, 427 
with thrombosis, 421 
clinical history, 422 

blanched condition of extremity in, 129 
bluish discoloration in, 129 
carbolic acid, 183 
chemical causes, 160 
classification, 160 



616 


INDEX OF SUBJECTS 


Gangrene, clinical examination in, 162 
coldness of extremity in, 129 
complicating aneurysms, 209 
infectious diseases, 203 
pneumonia, 481 
scleroderma, 561 
course and termination of, 159 
cyanosis in, 129 
definition, 127 
diabetic, 427 

diseases of blood vessels in, 161 
dry, 157, 158 

of one or more phalanges, 202 
due to chemicals and drugs, 181 
to ergot, 186 

to external or direct causes, 160 
to internal or indirect causes, 160 
to microbic agents, 160 
to neurogenic causes, 161 
to thermic causes, 160 
to poisonous gases, 184 
to pyogenic bacteria, 202 
embolic and thrombotic, after infectious 
diseases, 481 
clinical course, 481 
pathology, 483 
types of gangrene, 483 
arteriotomy in, 494 
technic, 498 

arteriovenous anastomosis in, 494 
diagnosis, 489 
embolectomy in, 494 
technic, 498 
ligation in, 494 
post-operative, 489 
treatment, 493 
complicating chorea, 485 
with cardiac disease, 485 
embolism in, 161 
embolism without, 480 
emphysematous, 190 
examination in, absence of pulsation as 
indication of arterial occlusion, 164 
angle of circulatory sufficiency in, 163 
appearance of limb, 162 
blanching in, 163 
color in, 163 
erythromelia in, 162 
in prodromal stages, 162 
ischemia in, 163 

reactionary hyperemia, rubor, or reac¬ 
tionary erythromelia in, 165 
rubor in, 162 

tests for circulation in, 165 
for patency of veins in, 168 
following injection of medicaments, 185 
of quinin, 185 
forms of, 157 
foudroyante, 190 

frequency of, after ligation of arteries 
at certain levels in lower extremities, 85 
gas, 190 

bacteriologic etiology, 190 
blood transfusion in, 201 
blood vessels in, 193 
diagnosis, 198 


Gangrene, gas, edema in, 197 
gangrene in, 198 
gas formation in, 197 
histogenic poisons of, 196 
incidence of, 194 
infection, epifascial form, 195 
superficial form, 195 
types of, 195 

latent infection with anaerobes, 194 
local medication in, 201 
symptoms, 197 
localization of, 195 
morbidity and mortality in, 199 
non-putrefactive type of bacteria hi, 190 
obstructive hyperemia in, 201 
oxygen insufflation in, 201 
pathogenesis of, 194 
pathological anatomy, 192 
period of incubation, 193 
putrefactive type of bacteria in, 191 
serum therapy, 201 
skin in, 197 

stages in development of, 193 
surgical treatment, 200 
symptoms, general, 196 
local, 197 
the wound in, 197 

toxins and antitoxin formatioh in, 190 
toxins of, 196 
treatment, 199 

with hyperemia, 200, 201 
vessel injury and, 198 
I general considerations, 127 
hospital, 187 

diphtheritic form, 186 
pulpy form, 188 
treatment, 188 
in recurrent fever, 203 
in typhoid fever, 203 
injuries to blood vessels and, 204 
injury of main nutrient vessels in, 160 
intermittent claudication in, 129 
ischemia in, 129 
line of demarcation in, 159 
mechanical causes, 160 
methods of investigation of, 130 
microbic, 157, 159, 160, 190 
moist, 157, 158, 392. 

characteristic clinical stages, 158 
multiple incisions for prevention of, 180 
neurotic, 567 

clinical course, 569 
etiology, 567 
hysteria in, 568 
of skin, 97, 98 
pathogenesis, 569 
prognosis, 569 
symptomatology, 568 
treatment, 570 

neurogenic, pathogenesis of, 98 
of fingers due to injection of arsphen- 
amin, 185 
Pott’s, 391 

premonitory symptoms, 128 
prodromal stages, examination in, 162 
puerperal, 485, 490 






INDEX OF SUBJECTS 


617 


Gangrene, putrid, 158 
redness of toes in, 129 
senile, 158, 391 

spontaneous amputation in, 159 
symptoms of impaired circulation in, 128 
thermic, 172 
causes of, 160 
clinical course, 174 
direct tissue injury in, 175 
effect of freezing in this type of gan¬ 
grene, 176 

effect of stasis in, 178 
etiology, 175 

freezing in, symptomatology, 173 
general consideration, 172 
internal causes, 175 
operative treatment, 181 
pathogenesis, 175 
predisposing factors in, 175 
prognosis, 180 
role of blood vessels in, 177 
thrombosis as cause of, 179 
treatment, 180 

vessel palsy in, importance of, 179 
tests for circulation in, 165 
thrombosis in, 129, 161 
thrombotic, in healthy or but slightly 
diseased vessels, 490 
peripheral, 572 
traumatic, 168 
causes, 168 

from accidental entombment, 170 
of an extremity, 170 
of deep tissues, with main arteries 
intact, 171 

of limited extent, 170 
superficial, with main vessels intact, 
171 

symptoms, 169 
treatment, 172 

with arterial thrombosis, 1.70 
without involvement of main arteries, 
I 7i 

trophic disorders in, 129 
with diphtheria, 484 
with other infections, 484 
without organic vascular disease, 539 
Gangrenous slough, 127 
stomatitis, 188 
Gas bacillus, 190 

infection, Van Beuren’s treatment, 199 
edema, 190, 191 

bacillus, Aschoff’s, 191 
formation in internal organs, 193 
gangrene, 190; see also Gangrene, gas. 
inflammation, 190 
phlegmon, 190 
local, 195 
progressive, 196 

Gases, poisonous, gangrene due to, 184 
Ghon-Sachs bacillus, 192 
Gigantism, acromegaly and, 530 
Glands, endocrine, functions of vegetative 
nervous system and, 502 
relation of, to vegetative nervous 
system, 55 


[ Gliosis spinalis and syringomyelia, 513 
Glossy skin, 97 
origin of, 96 

Glucose solution with adrenalin, injection 
of, gangrene following, 185 
Goldflam’s type of intermittent claudica¬ 
tion, 151 
Goose flesh, 505 
| Granular streaming, 66 
in capillaries, 586 
diagnosis, 469 

I Gumma, syphilitic tertiary, differential 
diagnosis, 469 

Hands, asphyxia of, 75 
cyanosis of, 75 
Heart, irritable, 59, 60 

acroasphyxia of, capillary pressure in, 
76 

asphyxia of, 75 

Hematoma, communicating, 208 
pulsating, 208 

Hemi-atrophy, progressive facial, 91 
Hemorrhages of vicarious menstruation, 79 
Henle-Coenen test for circulation, 168 
Herpes zoster, 96, 97, 513 
Heterologous stimulation, theory of, in 
trophic functions of nervous system, 94 
Histamin, effect of, on circulation, 61 
Hooker and Danzer’s method for capillary 
blood pressure estimation, 67 
Hormones, thyroid, importance of, in arte¬ 
rial affections, 502 
Hospital gangrene, 187 
diphtheritic form, 188 
pulpy form, 188 
treatment, 188 

Hot air treatment, in arteriosclerosis, 437 
Hyalin thrombi, 101 

Hydrochloric acid as cause of gangrene, 182 
Hyperemia, 73 
collateral, 82 
neuroparalytic, 73 

theory of, in trophic disorders, 91 
postanemic, 74 
reactionary, 156 
rubor, 75 
venous, 75 

consequences of, 75 
Hyperhidrosis in erythromelalgia, 532 
Hypersensitiveness of vegetative nervous 
system,-504 

Hypertrophy of arteries, 447 
Hyphemia, local, 71 

Hypophysis cerebri, effect of, on circula¬ 
tion, 56 

Hypoplasia of vascular system, congenital, 
as predisposing to vascular affections, 83 
Hypotension, arterial endocrine disease in, 
502 

Hypotonia, chronic, 70 
Hysterical pseudo tetanus, 143 

Idiopathic atrophy of skin, 566 
cutaneous atrophy, 504 
Illuminating gas, gangrene from, 184 




618 


INDEX OF SUBJECTS 


Impulses, antidromic, 37 
Incipient thrombo-angiitis obliterans with 
apparent vasomotor symptoms, 576 
Incisions, multiple, for prevention of 
gangrene, 180 

Indirect degeneration of nervous system, 94 
Induced rubor, 163 
Inflammation, gas, 190 
Inflammatory edema, 79 
Infection, gas bacillus, Van Beuren’s treat¬ 
ment, 199 

gangrene, types of, 195 
role of, in thrombosis, 126 
Infections, vasomotor and trophoneuroses 
following, 574 

Infectious agents, action of, in thrombus 
formation, 120, 121 
diseases, gangrene complicating, 203 
emboli, 479 

polyneuritis, vasomotor symptoms in, 521 
type of thrombosis, 108 
Influenza as cause of acute arteritis, 449 
Injuries to blood vessels, and gangrene, 204 
Innervation, antagonistic, of vessels, 34, 40 
vascular, double, recent views on, 38 
Instability, vasomotor, 570 
Insufficiency, vascular, 70 
in arteriosclerosis, 71 
Insulin in diabetic gangrene, 435 

in treatment of gangrene with hyper¬ 
glycemia, 442 

Intensive emotions, effects of, 513 
Interdependence of nerve paths with par¬ 
ticular reference to trophic function, 92 
Intermittent claudication, acute forms, 148 
age incidence, 152 

angioneurotic, with Raynaud’s disease 
of finger, 144 

angiospasm in, theories as to cause, 156 
artificial, 151 

as diagnostic symptom, 137 
Charcot-Erb type, 140 
circulatory and vasomotor phenomena 
in, 141 

clinical course, 142 
clinical types, 140 
critical summary, 154 
differential diagnosis, 157 
Erb type, characteristics, 137 
examination of pedal and crural 
arteries in, 142 

explanation of phenomena in, 155 
functional vasomotor type, 142 
historical, 139 
in gangrene, 129 
in other territories, 146 
in thrombo-angiitis obliterans, 255 
see also Thrombo-angiitis obliterans, 
intermittent claudication in. 
of inactivity, 136 
of spinal column, 146 
of upper extremities, 147 
of vasomotor type, 138 
organic type, relation of angiospasm to, 
144 

pathology, 151 


Intermittent claudication, Raynaud’s syn¬ 
drome and, differentiation, 138 
sex and race incidence, 153 
tobacco as etiologic factor in, 153 
type accompanying organic vascular 
disease, 139 

with healthy arteries, 155 
limping of horses, 140 
spasm of vascular capillaries, 144 
Internal organs, gas formation in, 193 
secretions and vegetative functions, 502 
circulation and, 55 
trophic disturbances and, 504 
Irritable heart, 59, 60 

acroasphyxia of, capillary pressure in, 
76 

asphyxia of, 75 

Irritants, thermic and actinic, cutaneous 
responses to, 509 
Ischemia, 71 

an index of circulation, 242 
causes, 71 

diminished arterial influx in, 72 
in gangrene, 129 

in thrombo-angiitis obliterans, 237; see 
also Thrombo-angiitis obliterans. 
local, consequences of, 73 
mechanical diminution of patency of 
arteries in, 72 

neuro-irritative, in trophic disorders, 91 
paradoxical, 84 

Ischemic contracture of muscles, without 
gangrene in blood vessel injury, 206 
degeneration, lesions of, following liga¬ 
tion of large or main arteries, 207 

Jacksonian epilepsy, vasomotor, 29 

Kalte-Gangran, 177 

Lactic acid, effect of, on blood vessels, 54 
Lenhossek cellifugal degeneration of ner¬ 
vous system, 92 
Leukodiapedesis, 77 
Leukocyte thrombus, 101 
Ligation of aneurysms, 211 

of femoral vein in treatment of thrombo¬ 
angiitis obliterans, 382 
Line of demarcation in gangrene, 159 
Linsenkernschlinge, 30 
Local anemia, 71 

circulation, pathological, 71 
freezing, symptomatology of, 173 
gas phlegmon, 195 
hypemia, 71 
shock, 526 

Localized asphyxia with arteries pulsating, 
572 

derangements of vascular tone, 70 
Lombard’s method of studying capillary 
circulation, 63 

Lymphatic system, disturbance in con¬ 
tinuity of vessel constituents, 79 
of capillary origin, 79 
functional derangement of, 79 
Lysol, gangrene from, 184 







INDEX OF SUBJECTS 


619 


Main succulent, 513 
Mai perforant, 97, 474 

alcohol in etiology, 477 
bone and joint theory, 477 
clinical course and symptoms, 477 
etiology, 475 

lesions of central nervous system 
in, 476 

local treatment, 479 
mechanical theory, 475 
nervous neurogenic theory, 475 
peripheral nerve lesions in, 475 
prognosis, 478 
treatment, 478 
vascular theory, 475 
plantaire perforant of Vesigne, 474 
Malfunction, nerve, causes, 81 
Malignant edema, bacillus of, 191 
Malum perforans pedis, 474 
Mask, sclerodermal, 562 
Matas test for circulation, 166 
Measure of blood flow in extremities, 49 
Mechanical stimuli, direct response of 
capillaries to, 60 

Medicaments, gangrene following injection 
of, 185 

Menstruation, vicarious, hemorrhages of, 79 
Mental symptoms in thrombo-angiitis 
obliterans, 270 

Mercurial poisons as cause of gangrene, 183 
Mercury as cause of gangrene, 183 
Metabolites, effect of, on blood vessels, 
54 

Metastatic thrombosis, 109 
Metatarsalgia, intermittent claudication 
and, differential diagnosis, 157 
Microbic gangrene, 157, 159, 160, 187, 190; 
see also Gangrene, microbic. 
poisons, gangrene from, 183 
Microcapillary tonometer, 67, 68 
Microscopy, capillary, 584; see also Capil¬ 
lary microscopy. 

Migrating arteritis, 305 
phlebitis, 214 

focal, of unknown origin, 470, 472 
in thrombo-angiitis obliterans, 279 
miscellaneous varieties, 470 
with infections, 472 
with pulmonary tuberculosis, 470 
Moist gangrene, 157, 158, 392 
Molecular death, 127 
Monoplegia, vasomotor, 29 
Morphea, 559 

Morphology of capillaries, 65 
in vasoneuroses, 595 
Mortification, 127 

Mosckowicz test for investigation of 
collateral circulation, 210 
for circulation, 166 

Motility, capillary, nerve influences in, 38 
Motor paralyses following arterial lesions, 
584 

Muller’s Zeiss apparatus for capillary 
microscopy, 587 . 

Muller-Weiss method of studying capillary 
circulation, 64 


Multiple neurotic gangrene, 567 
of skin, 97, 98 
Mummification, 127 

Muscular contracture, sympathetic and, 
relation of, 583 

Myasthenia gravis pseudo-paralytica, inter¬ 
mittent claudication and, differential 
diagnosis, 157 
paroxysmal, 155 

Myelitis, bullous eruptions in, 513 
Myositis, syphilitic, differential diagnosis, 
469 

Nails, alterations in, in thrombo-angiitis 
obliterans, 236 
trophic disorders of, 97 
Necrosis, 127 
colliquation, 183 
signs of, in a limited part, 128 
Nerve cells, role of, in production of trophic 
disturbances, 92 

control of capillary circulation, 59 
degeneration, interdependence of por¬ 
tions of nervous system in, 92 
disease, organic, Raynaud’s disease and, 
differentiation, 554 

distribution about common femoral 
artery, 36 

fibers, vegetative, course of, 23 
impulses and closed circuit, 91 
influences in capillary motility, 38 
on blood vessels, 95 
on osseous tissues, 94 
injury, complicating injuries to blood 
vessels, 206 

malfunction, causes, 81 
paths in skin, 506 

interdependence of, with particular 
reference to trophic function, 92 
sciatic, injury, 519 
Nerves of capillaries, 11 

peripheral, lesions of, irritative phe¬ 
nomena attending partial lesions, 
5 I 9 

symptoms with complete nerve 
destruction, 519 

vasomotor and trophic symptoms, 
520 _ 

following bullet wounds, 520 
vasomotor and trophic disorders in 
lesions of, 518 

sympathetic, causalgias of, treatment, 

523 

in relation to causalgia, 522 
painful lesions of, 522 
periarterial, neuroses and, 521 
vascular, centers, 44 
peripheral course of, 34 
vasoconstrictor, 36 
vasodilator, 37 

Nervous system, autonomic, 23 

central, vasomotor and trophic dis¬ 
turbances in lesions of, 513 
indirect degeneration of, 94 
interdependence of portions of, in 
nerve degeneration, 92 




620 


INDEX OF SUBJECTS 


Nervous system, Lenhossek cellifugal 
degeneration of, 92 
parasympathetic, 23, 28 
retrograde degeneration of, 93 
secondary atrophy of, 94 
sympathetic, 23, 25 

effect of adrenalin on, 580 
of calcium on, 581 
of ergotoxin on, 580 
pain and, 46 

role of, in certain pathologic condi¬ 
tions, 583 

in reflex contractures of Babinski- 
Froment type, 583 
spinal system and, relation of, 32 
trophic functions of, 90 
reflex theory of, 93 
theory of heterologous stimulation 
in, 94 

vasomotor, 22 

course of vegetative nerve fibers, 23 
effect of nicotin on, 579 
functions of, 36 
summary of, 46 

vegetative, cerebral lesions of, localiza^ 
tion of, 510 

diagnosis and localization of lesions 
of, 509 

effect of adrenalin on, 55 
hypersensitiveness of, 504 
internal secretions and, 502 
neuroses of, theoretical concept of, 

5 QI 

pharmacologic tests of functions of, 

512 

relation of endocrine glands to, 55 
skin and, 504 

Wallerian degeneration of, 92 
Neuralgia due to cold, 174 
Neuritis complicating injury to blood¬ 
vessels, 206 

intermittent claudication and, differen¬ 
tial diagnosis, 157 

Neurogenic gangrene, pathogenesis of, 98 
Neuro-irritative anemia, 72 

ischemia in trophic disturbances, 91 
Neuroparalytic hyperemia, 73 

theory of, in trophic disorders, 91 
Neuroses of vegetative nervous system, 
theoretical concept of, 501 
periarterial, sympathetic nerves and, 521 
traumatic, with vasomotor disturbances 
of hands and feet, 574 
vasomotor and trophic, general consider¬ 
ations, 499 

as prodromal stage of thrombo-angiitis 
obliterans, 574 
atypical, 572 

capillary microscopy in, 590 
circulatory, Raynaud’s disease and, 
differentiation, 554 
surgical treatment, 581 
operation, 582 

thrombo-angiitis and, differential diag¬ 
nosis, 375 

treatment, 578 


Neurotic gangrene, multiple, 567 
of skin, 97, 98 

Neurotrophic disorders in spina bifida, 514 
of skin, 96 

influences, exercise of, 91 
skin changes in syringomyelia, 97 
Neurovascular syndromes after ligation of 
large arteries, 212 
Newborn, sclerema of, 559 
Nicotin, action of, upon ganglion cells, 23 
as causal factor in atherosclerosis, 22 
effect of, on vasomotor nervous system, 
579 

Nitric acid as cause of gangrene, 182 
Noma, 188 

treatment, 189 
Normal anastomoses, 10 
Nuclei in corpus striatum, 31 
Nucleus sympatheticus lateralis inferior, 25 
superior, 25 
medialis inferior, 25 

Obstructive vascular disease, demonstra¬ 
tion of collaterals in, 84 
Obturation, arterial, without immediate 
symptoms, 480 

Occlusion, vascular, of doubtful origin, 472 
Occlusive thrombi, absence of pulsation 
distal to, 134 

Oppenheim’s type of intermittent claudica¬ 
tion, 142 

Organic arterial disease, Raynaud’s disease 
and, differentiation, 557 
vasoneurosis and, 578 
nerve disease, Raynaud’s disease and, 
differentiation, 554 

obstructive arterial diseases, pain in, 136 
vascular disease, gangrene without, 539 
Organs, internal, gas formation in, 193 
Orthoform as cause of gangrene, 183 
Osseous changes in thrombo-angiitis 
obliterans, 275 

tissues, nerve influences on, 94 
Oxalic acid as cause of gangrene, 182 

Pain as diagnostic symptom, 135 
in ervthromelalgia, 135, 531 
in organic obstructive arterial diseases, 
136 

in Raynaud’s disease, 135, 549 
in thrombo-angiitis obliterans, 135, 258; 
see also Thrombo-angiitis obliterans , 
pain in. 

in trophic disorders, 137 
induced by prolonged pendency of limb, 
I 3 6 

paroxysmal, of diffuse variety, 136 
referred, 135 

sympathetic nervous system and, 46 
Painful lesions of sympathetic nerves, 522 
Pallor, 73 
artificial, 151 

Palpation of anterior tibial artery, 10 
of axillary artery, 5 
of brachial artery, 5 
of dorsalis pedis artery, 10 




INDEX OF SUBJECTS 


621 


Palpation of femoral artery, 6 
of popliteal artery, 7, 9 
of radial and ulnar arteries, 5, 6 
Papillary pressure, variations in, in capil¬ 
laries, 594 

Paradoxical ischemia, 84 

Paralyses, motor, following arterial lesions, 

584 

Paralysis douleureuse ischemique, 140 
Paralytic action of poisons on capillaries, 61 
Parasympathetic nervous system, 23, 28 
Paratyphus bacillus, 203 
Paredema bacillus, Pfeiffer-Bessau, 191 
Parietal arteritis, 451 
Paroxysmal myasthenia, 155 
pain of diffuse variety, 136 
Patency of veins, tests for, 168 
Periarterial sympathetic nerves, cutting of, 
characteristic signs following, 582 
neuroses and, 521 
Periarteritis, 455 
nodosa, 462 

clinical manifestations, 463 
manifestations in extremities, 463 
thrombus formation in, 122 
Peripheral arteriosclerosis, 71 

circulation, elementary principles, 48 
functional disturbances of, 76 

due to derangement of capillary 
flow, 76 

to impaired exchange of fluids, 78 
physiology of, 48 
course of vascular nerves, 34 
nerve lesions, irritative phenomena at¬ 
tending partial nerve lesions, 519 
symptoms with complete nerve 
destruction, 519 

vasomotor and trophic disorders in, 
518 

symptoms, 528 

following bullet wounds, 520 
parasympathetic and sympathetic fibers, 
antagonistic influence of, on single 
vegetative organs, 43 
thrombotic gangrene, 572 
venopressor mechanism, 59 
Pfeiffer-Bessau bacillus, 191 
paredema bacillus, 191 
Phalanges, dry gangrene of one or more, 202 
Pharmacologic tests of vegetative functions, 
5 12 

Phlebitis, extensive recurring, 472 
migrating, 214 

focal, of unknown origin, 470, 472 
in thrombo-angiitis obliterans, 279 
miscellaneous varieties, 470 
with infections, 472 
with pulmonary tuberculosis, 470 
rheumatic, 452 

rheumatismal, differential diagnosis, 469 
syphilitic, diagnosis of, 469 
tertiary, histopathology of, 469 
Phlebosclerosis, 420 
Phlegmon, gas, 190 
local, 195 
progressive, 196 


Phosphorus as cause of gangrene, 183 
Physiology of capillaries, 57 
of peripheral circulation, 48 
of vasomotor centers, 41 
recent views on, 43 
Pigmentation in scleroderma, 560 
Pilocarpin, effect of, on vegetative func¬ 
tions, 512 

Pituitrin, effect of, on circulation, 56 
Platelet thrombus, 106 

cause of development of, 107 
Pneumonia, gangrene complicating, 481 
Poison of bees and wasps, gangrene from, 

183 

Poisonous gases, gangrene due to, 184 
Poisons, endogenous, in thrombosis, 119 
exogenous, and infectious agents, action 
of, in thrombus formation, 120 
in thrombosis, 120 
microbic, gangrene from, 183 
paralytic action of, on capillaries, 61 
selective action of, on sympathetic and 
parasympathetic systems, 580 
Polyneuritis, infectious, vasomotor symp¬ 
toms in, 521 

Raynaud’s disease and, differentiation, 
554 

Popliteal artery, anatomy, 7 

palpation of, Buerger’s method, 133 
pulse, 8 

manner of detecting, 132 
Postanemic diapedesis, 77 
hyperemia, 74 

Postural treatment, Buerger’s, 77 
Pott’s gangrene, 391 
Precipitation thrombosis, 108, no 
Primary coagulation thrombosis, 108 
Progressive facial hemi-atrophy, 91 
gas phlegmon, 196 
Proserozym, 103 
Pseudo-aneurysms, 208 
Pseudophthisis, 425 
Pseudo tetanus, hysterical, 143 
Psychoneurosis, vasomotor, 574 
Puerperal gangrene, 485, 490 
thrombosis, 108 

Pulmonary tuberculosis with phlebitis 
migrans, 470 

Pulpy form of hospital gangrene, 188 
Pulsating hematoma, 208 
Pulsation, absence of, distal to occlusive 
thrombi, 134 
in gangrene, 129 

arterial, as diagnostic symptom, 132 
in Raynaud’s disease, 550 
in thrombo-angiitis obliterans, 263; 
see also Thrombo-angiitis obliterans, 
arterial pulsation in. 

Pulse, axillary, 5 
brachial, 5 
dorsalis pedis, 10 
femoral, 7 
popliteal, 8 

manner of detecting, 132 
radial, 6 
tibial, 10 




622 


INDEX OF SUBJECTS 


Pulse, ulnar, 5 
vagus, 44 

Pulsion thrombosis, hi, 117 

Putrid gangrene, 158 

Pyogenic bacteria, gangrene due to, 202 

Quinin, injection of, gangrene following, 

185 

Radial artery, anatomy, 5, 6 
pulse, 6 

Raynaud’s disease, 542 

acroasphyxia chronica and, differentia¬ 
tion, 554 

acrocyanosis in, 71, 72 
acroparesthesiae of Schultze and, differ¬ 
entiation, 553 
arterial pulsation in, 550 
capillary microscopy in, 599 
clinical picture, 543 
demonstrable phenomena in, 550 
diagnosis, 553 

differentiation from vasomotor and 
trophic neuroses, 553 
erythromelalgia and, differential diag¬ 
nosis, S'n 
etiology, 545 

evidences of vasomotor instability in, 
550 

incidence, 544 
local asphyxia in, 546 
local syncope in, 546 
nomenclature, 544 

of finger, with angioneurotic inter¬ 
mittent claudication, 144 
organic arterial diseases and, differ¬ 
entiation, 557 
osseous changes in, 548 
pain in, 135, 549 
pathology,. 552 

polyneuritis and, differentiation, 544 
remote clinical phenomena in, 550 
sclerodactyly and, differential diagno¬ 
sis, 552 

scleroderma, and sclerodactyly, 551 
sensory symptoms in, 549 
simple vasomotor circulatory neuroses 
and, differentiation, 554 
spasms of capillaries in, 67 
stage of vasomotor phenomena in, 
546 

symptomatology, 546 
syringomyelia and, differentiation, 555 
thrombo-angiitis obliterans and, differ¬ 
entiation, 555 
treatment, 558 

trophic disorders and gangrene in, 547 
vascular disease and, differentiation, 
.555 

Reactionary hyperemia, 156 
rubor, 163 

Recurrent fever, gangrene in, 203 
Redness of toes in gangrene, 129 
Referred pain, 135 

Reflex theory of trophic functions of 
nervous system, 93 


Reflexes, axon, 37 
vaso-vasomotor, 45 
vegetative, in skin, 505 
viscero-vasomotor, 45 

Refrigeration, local, effects of, in thrombus 
formation, 123 

Responses, vasomotor and autonomic, 53 
Rete patellae, 86 

Retrograde degeneration of nervous system, 
93 

Rheumatic arteritis, 451 
phlebitis, 452 

Rheumatismal phlebitis, differential diag¬ 
nosis, 469 
Rubor, 89 

and cyanosis, 573 
chronic, 163 
hyperemia, 74 
induced, 163 

involving toes in gangrene, 129 
reactionary, 163 

Schienbein Schmerz, 173 
Schultze, acroparesthesiae of, Raynaud’s 
disease and, differentiation, 553 
Sciatic nerve injury, 519 
Sciatica, intermittent claudication and, 
differential diagnosis, 157 
Sclerema neonatorum, 559 
Sclerodactyly, 378, 559, 563 

Raynaud’s disease and, differential diag¬ 
nosis, 552 

scleroderma and Raynaud’s disease, 551 
Scleroderma, 559 
clinical course, 564 

deranged internal secretions in, 502, 503 
diagnosis, 565 
disturbed motility in, 562 
gangrene complicating, 561 
general symptoms, 563 
joint lesions complicating, 563 
mucous membranes in, 563 
neurogenic theory in, 565 
osseous changes complicating, 562 
pathogenesis, 564 
pigmentation in, 560 
prognosis, 566 
secretory changes in, 560 
sensory disturbances in, 562 
sclerodactyly, and Raynaud’s disease, 551 
symptomatology, 560 
symptoms of erythromelalgia associated 
with, 563 

theory of malfunction of endocrine glands 
in, 564 

thyroid imbalance theory in, 564 
treatment, 566 
trophic disturbances in, 561 
true, thrombosis-angiitis obliterans and, 
differential diagnosis, 378 
vascular theory in, 565 
vasomotor disturbances in, 561 
symptoms in, 563 
Sclerodermal mask, 562 
Sclerotic arteries, bone formation in, 421 
Secondary atrophy of nervous system, 94 



INDEX OF SUBJECTS 


623 


Secretions, internal, and vegetative func¬ 
tions, 502 
circulation and, 55 
trophic disturbances and, 504 
Senile changes in arteries, 19 
gangrene, 158, 391 
Sepsis, anaerobic, 196 
Serozym, 103 

Serpent venom, gangrene from, 183 
Serum therapy in gas gangrene, 201 
Shock, 62 
local, 526 

Silver nitrate as cause of gangrene, 183 
Skin changes, neurotrophic, in syringo¬ 
myelia, 97 
composition of, 584 
glossy, 97 
origin of, 96 
histology of, 584 
idiopathic atrophy of, 566 
lesions due to trophoneurotic causes, 97 
multiple neurotic gangrene of, 97, 98 
nerve paths in, 506 
trophic disorders of, 96 
summary, 99 
vascularization of, 585 
vasomotor phenomena of, 506 
vegetative nervous system and, 504 
reflexes in, 505 
Slough, gangrenous, 127 
Sloughing, 127 
Sloughs, 127 

Sodium chlorid injection of, gangrene 
following, 185 

Spasm and atony of capillaries, 592 
arterial, 77 

intermittent, of vascular capillaries, 144 
of vasconstrictors following bullet 
wounds, 206 
—ofvenules, 77 
traumatic vasomotor, 523 
treatment, 525 

Spasmophilic conditions, altered calcium 
metabolism in, 580 

Spasm of capillaries in Raynaud’s dis¬ 
ease, 67 

Spastic anemia, 72 
Sphacelation, 127 

Sphacelinic acid, gangrene from, 186 
Sphacelus, 127 

Spina bifida occulta, disturbances due to 
lesions of nerve apparatus, 516 
local symptoms, 515 
nerve lesions of cord or cauda 
equina in, 515 

neurotrophic disorders in, 514 
symptoms, 515 

vasomotor and trophic disturbances 
in, 516 

Spinal column, intermittent claudication 
of, 146 

cord injuries, vasomotor disturbances 
in, 514 

vasomotor paths in, 32 
nerves, sympathetic nervous system and, 
relation of, 32 


Spinal vasomotor centers, 31 
Spodogenic thrombi, 101, 118 
thrombosis, no 
Spontan-Gangran, 307 
Spontaneous amputation in gangrene, 159 
Stagnation thrombosis, m, 116 
thrombus, no 

Stases in capillary circulation, 589 
Stewart’s method of measuring blood flow, 
5 ° 

Stimuli, chemical, direct response of capil¬ 
laries to, 60 

mechanical, direct response of capillaries 
to, 60 

Stomatitis, gangrenous, 188 
Stream and pressure conditions in vaso- 
neurotic diathesis, 592 
Streaming, granular, 66 
in capillaries, 586 
Subcortical vasomotor centers, 30 
Sulphuric acid as cause of gangrene, 182 
Superficial circulation, in obstructive vas¬ 
cular diseases, 80 
changes in vasomotor mech¬ 
anism in, 81 

chemical action on tissues in, 81 
diminished force of stream in, 80 
exhaustion in, 81 
hydrostatic and gravity forces 
in, 80 

Sympathectomy, periarterial, characteristic 
signs following, 582 

Sympathetic and peripheral parasympa¬ 
thetic fibers, antagonistic influence of, 
on single vegetative organs, 43 
nerve, periarterial, cutting of, charac¬ 
teristic signs following, 582 
nerves, causalgias of, treatment, 523 
in relation to causalgia, 522 
painful lesions of, 522 
periarterial, neuroses and, 521 
nervous system, 23, 25 

effect of adrenalin on, 580 
of calcium on, 581 
of ergo toxin on, 580 
pain and, 46 

role of, in certain pathologic con¬ 
ditions, 583 

in reflex contractures of Babinski- 
Froment type, 583 
spinal system and, relations of, 32 
Symptoms, diagnostic; see Diagnostic symp¬ 
toms. 

Syndrome, Erb’s, 129 
Synesthesalgia, 523 
Syphilis, thrombus formation in, 121 
Syphilitic arteritis and gangrene, 456 
clinical forms, 460 
incidence, 459 
pathology, 456 
symptomatology, 460 
disease of veins, 464 

clinical characteristics, 464 
histopathology of tertiary phlebitis, 
469 

pathology, 464 







624 


INDEX OF SUBJECTS 


Syphilitic disease of veins, tertiary or late 
form, 468 
thrombus in, 468 

gumma of veins, differential diagnosis, 

469 

tertiary, differential diagnosis, 469 
myositis, differential diagnosis, 469 
phlebitis, diagnosis of, 469 
Syringomyelia and gliosis spinalis, 513 
neurotrophic skin changes in, 97 
Raynaud’s disease and, differentiation, 
555 

Tabes dorsalis, trophic disturbances in, 513 
Taches cerebrales, 74 

Tarsalgia and intermittent claudication, 
differential diagnosis, 157 
Tertiary phlebitis, histopathology of, 469 
Test, compression, 77 
expression, 163 

Henle-Coenen, for circulation, 168 
Matas, for circulation, 166 
Moskowicz, for circulation, 166 
Tests for circulation, 165 

value of, in thrombo-angiitis oblit¬ 
erans, 167 

for patency of veins, 168 
pharmacologic, of vegetative functions, 
5 12 

Tetany, altered calcium metabolism in, 580 
T heoretical concept of neuroses of vege¬ 
tative nervous system, 501 
Therapeutic development of collaterals, 87 
Thermic gangrene, 172; see also Gangrene, 
thermic. 

Thermic causes of gangrene, 160 
influences, thrombosis due to, 122 
irritants, cutaneous responses to, 509 
Thrombi, appearance of, 105 
cause of formation, 101 
forms of, 100 
hyalin, 101 
leukocyte, 101 
mixed, 101 

occlusive, absence of pulsation distal to, 
134 

red, 101 

spodogenic, 101, 118 
types of, 101 
white, 101 

Thrombo-angiitis obliterans, 81, 213 
acute stage, 149, 218 
acute symptoms, 218 
alterations in nails in, 236 
appearance of limb in, 235 
arterial pulsation in, 263 
absent pulses, 263 
cases with insignificant symptoms, 
265 

one or both limbs compro¬ 
mised early and lost, 266 
disappearance of pulses com¬ 
patible with arrested symptoms, 
267 

importance of popliteal pulse, 267 
in certain early cases, 263 


Thrombo-angiitis obliterans, arterial pulsa¬ 
tion absent in all arteries of a 
limb, 264 

and angle of circulatory suffi¬ 
ciency in, 269 

pulsations disappearing under ob¬ 
servation, 266 

pulses of upper extremities, 269 
present, 266 

relation of pulsation and clinical 
duration, 269 
return of pulsation, 269 
sequence of loss of pulsation in, 268 
severity of symptoms correspond¬ 
ing to arterial occlusion, 267 
arteriosclerosis associated with, 306 
simulating, 431 

arteritis with thrombosis simulating, 
454 

as borderline case, 576 
chemical action in, 82 
chronic stage, 219 

arrested stage or temporary heal¬ 
ing in, 229 

cases in elderly individuals, 228 
in females, 226 

in young with grave prognosis, 

224 

losing the limb last affected, 222 
of exquisite chronic rubor, 219 
of long duration without trophic 

lesions, 224 

of short duration, acute and 
subacute, 220 

with all extremities involved, 

225 

with all vessels pulsating, 226 
with apparent healing or cure, 

228 

with chronic course in one limb, 
acute course in other, 223 
with intermittent claudication 
and migrating phlebitis only, 

221 

with intermittent claudication 
only, 221 

with lethal outcome, 224 
with pain only, 225 
without symptoms, 220 
without tropic disorder or gan¬ 
grene requiring amputation, 
225 

without trophic lesions or gan¬ 
grene, 219 
doubtful cases, 231 
relapsing cases, 223 
sudden gangrene simulating em¬ 
bolic type, 220 

trophic lesions first symptom, 220 
classification, 231 
clinical concept, 214 
picture, 231 
coldness in, 261 

directly attributable to vascular 
occlusion, 262 
neurotic types, 261 






INDEX OF SUBJECTS 


625 


Thromboangiitis obliterans, coldness in, 
prolonged vasomotor and hydro¬ 
static coldness with ischemia, 261 
transitory vasomotor, 261 
cyanosis in, 250 
local chronic, 251 
pathogenesis of, 253 
temperature conditions in, 252 
diagnosis, 374 
clinical, 375 

differential, from true scleroderma, 
378 

from vasomotor neuroses, 375 
symptoms characteristic of, 374 
early, 576 
edema in, 254 

persistent, harbinger of gangrene, 
255 

erythromelalgia and, differential diag¬ 
nosis, 534 

erythromelia in, 215, 242 

action of specific toxins in, 249, 250 
chronic, 243 

duration of, 245 
exhaustion of vasoconstrictor 
mechanism in, 249 
explanation of, 247 
inflammatory, 242 
intrinsic, 243 

local action of metabolites or katab- 
olic agents in, 249, 250 
reactionary or induced, 243 
significance of, 245 
types of, 242 
vasomotor, 245 
etiology, 277 
fissures of soles in, 236 
gross pathology, 311 
histopathology, 314, 321 

acute lesion in deep vessels, 334 
elastic tissue in, 358 
healed or old stage, 338 
in acute or specific lesions, 317 
stage of disease, 321 
in healed or organized stage, 316 
intermediate stage of healing, 337 
pathology of the relapsing lesion, 

354 , 

specific lesions in deep vessels, 334 
terminations of occluding tissue, 350 
incipient, with apparent vasomotor 
symptoms, 576 

intermittent claudication in, 214, 255 
vasomotor symptoms with, 256 
with pulsating arteries, 256 
introduction, 213 

involvement of upper extremities, 294 
early symptoms of, 294 
simulating scleroderma and 
sclerodactyly, 305 
with acute arteritis of portions 
radial and ulnar arteries, 305 
with atrophy and gangrene, 303 
with extensive gangrene, 302 
with gangrene of slight extent, 
300 


Thrombo-angiitis obliterans, involvement 
of upper extremities with 
lesions simulating neurogenic 
disturbances, 297 
with trophic and vasomotor 
phenomena, 299 
with trophic disorders only, 299 
with vasomotor symptoms pre¬ 
dominating, 295 
without subjective symptoms, 
295 

ischemia in, 215, 237 

an index of circulation, 242 
mechanical or hydrostatic type, 237 
angle of elevation that pro¬ 
duces it, 238 

arc or angle in which it per¬ 
sists, 248 
extent of, 239 

obstinate areas of pallor in, 
240 

situation of its appearance, 238 
time interval of its establish¬ 
ment, 239 

vasomotor type, 240 
mental symptoms in, 270 
migrating phlebitis in, 279 

both playing equally important 
roles in symptom-complex, 284 
cases in which absolute evidences 
of deep arterial involvement 
are lacking, 291 

with symptoms of limited vein 
involvement, 280 
without symptoms, 280 
causing patient to seek treatment, 
281 

conclusions from vein lesions, 292 
extensive fulminating, 291 
involving both upper and lower 
extremities, 286 
mottling of skin in, 236 
neurotic types, 261 
of lower extremities, 232 
forms of onset, 232 
unusual clinical pictures in, 234 
osseous changes in, 275 
pain in, 135, 258 

continuous, in toes, 260 
sequence of various types, 260 
varieties of, 258 
pathological concept, 214 
pathology, 307 

in accidental exitus, 369 
in cases with slow termination, 371 
in lethal cases, 368 

predisposition to thrombosis in etiology 
of, 278 

Raynaud’s disease and, differentiation, 
555 . 

rubor in, 215 

scleroderma and, differential diagno¬ 
sis, 378 

statistical data, 276 
syphilitic phlebitis and, differential 
diagnosis, 469 


40 









626 


INDEX OF SUBJECTS 


Thrombo-angiitis obliterans, tenderness in, I 
260 

thrombosis in, 109 
treatment, 378 
conservative, 380 

diathermic, for enhancing circula- ! 
tion, 380 

heat for enhancing circulation, 381 1 
intermittent compression of main 
arteries for enhancing circula- ' 
tion, 382 

internal medication, 382 
local, 382 

methods of enhancing circula- j 
tion, 380 

postural method for enhancing 
circulation, 380 

• subcutaneous or intravenous in- j 
jection of solutions for enhanc- [ 
ing circulation, 381 
of pain, 379 
operative, 382 

arteriovenous anastomosis, 382 
ligation of femoral vein, 382 > 
limited amputation, 383 
radical amputation, 383 
prophylactic, 379 

selection of therapeutic procedures, 

384 

value of tests for circulation in, 167 | 
vasomotor neuroses and, differential i 
diagnosis, 375 
as prodromal stage of, 574 
vasomotor symptoms in, 271 

evidences of altered function 
in, 274 

in early stages only, 273 
syncope or ischemia after exertion, I 
273 

without pain, 258 
Thrombophilia, 126 
Thrombophlebitis, 214 

associated with thrombo angiitis oblit¬ 
erans causing patient to seek treat¬ 
ment, 282 

cases in which absolute evidences of deep 
arterial involvement are lacking, 291 
extensive fulminating type, in thrombo¬ 
angiitis obliterans, 291 
involving both upper and lower extremi¬ 
ties, in thrombo-angiitis obliterans, 286 j 
thrombo-angiitis obliterans and, both j 
playing equally important roles in 
symptom-complex, 284 
with symptoms of limited vein involve¬ 
ment in thrombo-angiitis obliterans, 280 
without symptoms in thrombo-angiitis 
obliterans, 280 

Thrombosis and embolism, 479 

arterial obturation without immediate ! 

symptoms, 480 
classification, 479 
complicating arteriosclerosis, 493 
in acute aortitis, 493 
and general diseases, 123 
arterial, with traumatic gangrene, 170 


Thrombosis, arteriosclerotic gangrene with, 
clinical history, 422 

as cause of gangrene after freezing, 179 
chemical alterations of total blood 
in, 124 
varieties, 119 
coagulation, 101 
conglutination, 101 
distant, 109 

due to actinic causes, 123 
to solid bodies, 122 
to thermic influences, 122 
effects of local refrigeration, 123 
endogenous poisons in, 119 
exogenous poisons in, 120 
general causes, 123 
general considerations of, 100 
in gangrene, 129, 161 
in thrombo-angiitis obliterans, 109 
increased viscosity of blood in, 125 
mechanical types of, hi 
metastatic, 109 
of cachectic conditions, 125 
of chemical origin, 118 

inflammatory processes in, 119 
of larger more central paths with arterio¬ 
sclerosis, 424 

physical explanations of, 105 
precipitation, 108, no 
primary coagulation, 108 
process of, classification of, no 
process of, coagulation in, 108 
puerperal, 108 
pulsion, in, 117 
relation of, to age, 125 
role of infection in, 126 
special conditions in, 125 
spodogenic, no 
stagnation, in, 116 
types of, 100 

with arteriosclerosis atrophy as sequel, 

425 

clinical course, 421 
diagnosticated as acute intermittent 
claudication, 150 

with arteritis simulating thrombo-angiitis 
obliterans, 454 

Thrombotic and embolic gangrene after 
infectious diseases, 481 
clinical course, 481 
pathology, 483 
types of gangrene, 483 
arteriotomy in, 494 
technic, 498 

arteriovenous anastomosis in, 494 
diagnosis, 489 
embolectomy in, 494 
technic, 498 
ligation in, 494 
post-operative, 489 
treatment, 493 

gangrene in healthy or but slightly 
diseased vessels, 490 
peripheral gangrene, 572 
Thrombus, accretion, no 
formation, 106 






INDEX OF SUBJECTS 627 


Thrombus formation, bacteria in, 120 

coagulation and agglutination in, 102 
congelation in, 105 
determining factor in, 100 
forces engaged in, 102 
in peri-arteritis nodosa, 122 
in syphilis, 121 
in tuberculosis, 121, 122 
in vessels implicated in war wounds, 
205 

platelet, 106 

cause of development of, 107 
stagnation, no 

Thyroid hormones, importance of, in 
arterial affections, 502 
Tibial artery, anterior, anatomy, 10 
posterior, anatomy, 9 

and vein, normal, characteristics, 18 
pulse, 10 

Tissues, osseous, nerve influences on, 94 
Tobacco as etiologic factor in intermittent 
claudication, 153 

as predisposing factor in thrombo¬ 
angiitis obliterans, 278, 279 
Toes, bluish discoloration of, in gangrene, 
129 

redness of, in gangrene, 129 
Tonometer, microcapillary, 67, 68 
Tonus, vascular, localized derangements 
of, 70 

vasomotor, 42 

Toxins and antitoxin formation in gas 
gangrene, 190 
of gas gangrene, 196 
Traumatic aneurysms, 208 
decubitus, acute, 170 
gangrene, 168; see also Gangrene , trau¬ 
matic. 

neuroses with vasomotor disturbances 
of hands and feet, 574 
vasomotor spasm, 523 
treatment, 525 
Trophedema, 98 

Trophic and vasomotor disorders in lesions 
of central nervous system, 513 
in peripheral nerve lesions, 518 
neuroses, general considerations, 499 
disorders and gangrene in arteriosclerotic 
disease, 390 
clinical forms of, 393 
in gangrene, 129 
internal secretions and, 504 
of nails, 97 
of skin, 96 
summary, 99 
pain in, 137 

slight, with vasomotor symptoms, 573 
function, independence of nerve paths, 
with reference to, 92 
of nervous system, 90 
reflex theory of, 93 
theory of heterologous stimulation 
in, 94 

influences of nerves on blood vessels, 95 
nerves, special, theory of, in trophic 
disorders, 91 


Trophoneuroses and vasomotor neuroses 
following infections, 574 
Trophoneurotic causes, skin lesions due to, 
97 

True aneurysms, 208 

Trunk and extremities, vasomotor paths of, 
5 11 

Tuberculosis of arteries, 455 

pulmonary, with phlebitis migrans, 470 
thrombus formation in, 121, 122 
Tuberculous endarteritis, 456 
Typhoid fever, gangrene in, 203 

Uhrzeigerbazillus, 191 
Ulceration, 127 
Ulnar artery, anatomy, 5 
pulse, 5 
Urticaria, 96 
gangrenosa, 570 

Vagus pulse, 44 

Van Beuren’s treatment of gas bacillus 
infection, 199 

Vascular affections, congenital hypoplasia 
of vascular system predisposing to, 83 
capillaries, intermittent spasm of, 144 
crises, 70 

disease, obstructive, demonstration of 
collaterals in, 84 

organic, chronic acroasphyxia and, 
differential diagnosis, 531 
gangrene without, 539 
Raynaud’s disease and, differentiation, 
555 . 

innervation, double, recent views on, 38 
insufficiency, 70 

in arteriosclerosis, 71 
nerve centers, 44 
nerves, peripheral course of, 34 
occlusion of doubtful origin, 472 
system, congenital hypoplasia of, as 
predisposing to vascular affections, 83 
tone, localized derangements of, 70 
Vascularization of skin, 585 
Vasoconstriction as sequence to obstructive 
anemia, 74 

Vasoconstrictor nerves, 36 
Vasoconstrictors, spasm of, following bullet 
wounds, 206 
Vasodilatation, 53 

as sequence to obstructive anemia, 74 
Vasodilator function, 40 
nerves, 37 

Vasomotor and autonomic responses, 53 
and trophic disorders in lesions of central 
nervous system, 513 
in peripheral nerve lesions, 518 
neuroses, following infections, 574 
general considerations, 499 
centers, cerebral, 28 
physiology of, 41 
spinal, 31 
subcortical, 30 

circulatory neuroses, Raynaud’s disease 
and, differentiation, 554 





628 


INDEX OF SUBJECTS 


Vasomotor disturbances of hands and feet, 
traumatic neuroses with, 574 
function and circulation, 52 
instability, 570 
Jacksonian epilepsy, 29 
monoplegia, 29 
nervous system, 22 

course of vegetative nerve fibers, 23 
effect of nicotin on, 579 
functions of, 36 
summary of, 46 

neuroses and organic arterial disease, 
578 

as prodromal stage of thrombo-angntis 
obliterans, 574 
atypical, 572 

capillary microscopy in, 590 
morphology of capillaries in, 595 
nature of, 591 
surgical treatment, 581 
operation, 582 

thrombo-angiitis obliterans and, differ¬ 
ential diagnosis, 375 
treatment, 579 

paths for trunk and extremities, 511 
in spinal cord, 32 

phenomena in arteriosclerotic disease, 
399 

of skin, 506 
psychoneurosis, 574 
spasm, traumatic, 523 
treatment, 525 

symptoms in infectious polyneuritis, 521 
in thrombo-angiitis obliterans, 271 
with slight trophic disorders, 573 
tonus, 42 

type of intermittent claudication, 142 
Vasoneuroses; see Vasomotor neuroses. 
Vasoneurotic constitution, 571, 590 
diathesis, 590 

fullness of capillaries in, 594 
stream and pressure conditions in, 592 
Vaso-vasomotor reflexes, 45 
Vegetative functions, internal secretions 
and, 502 

pharmacologic tests of, 512 
nervous system, cerebral lesions of, 
localization of, 510 
diagnosis and localization of lesions 
of, 509 

effect of adrenalin on, 55 
hypersensitiveness of, 504 


Vegetative nervous system, internal secre¬ 
tions and, 502 

neuroses of, theoretical concept of, 

5 01 

pharmacologic tests of functions of, 
5 12 

relation of endocrine glands to, 55 
skin and, 504 
reflexes in skin, 505 
Vein, axillary, 5 

femoral, ligation of, in treatment of 
thrombo-angiitis obliterans, 382 
Veins, patency of, tests for, 168 
syphilitic disease of, 464 

clinical characteristics, 464 
histopathology of tertiary phlebitis, 
469 

pathology, 464 
tertiary or late form, 468 
thrombus in, 468 

gumma of, differential diagnosis, 469 
Venom, serpent, gangrene from, 183 
Venopressor mechanism, peripheral, 59 
Venous hyperemia, 75 
consequences of, 75 
Venules, anatomy, 12 
spasm of, 77 

Vessel injury and gas gangrene, 198 
Vessels, antagonistic innervation of, 34 
Vicarious menstruation, hemorrhages of, 79 
Viscero-vasomotor reflexes, 45 
Visualization of capillaries, apparatus for, 
586 

von Hibler bacillus, 191 

Wallerian degeneration in nervous sys¬ 
tem, 92 

War edema, 70 

Wasps and bees, poisons of, gangrene from, 

183 

Weiss and Dieter’s method of studying 
capillary circulation, 64 
Weiss-Miiller method of studying capillary 
circulation, 64 
Welch gas bacillus, 190 
Wounds, bullet, of peripheral nerves, vaso¬ 
motor and trophic symptoms follow¬ 
ing, 520 

spasm of vasoconstrictors following, 
206 

war, thrombus formation in vessels 
implicated in, 205 



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